Infections Of Bone And Joint

Published on 16/03/2015 by admin

Filed under Orthopaedics

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1418 times

Chapter 13 Infections of Bone and Joint

Although bone and joint infection remains a serious problem, acute, fulminating bone involvement is seen much less frequently than in the past. The cause of these disorders is usually bacterial. Although more effective antibiotics continue to be developed, treatment of the established chronic infection remains a challenging problem.

Acute Osteomyelitis

Osteomyelitis is an infection of the bone or bone marrow. It is often classified as either acute, subacute, or chronic. Acute and subacute osteomyelitis are usually disorders of childhood and are less common in adults. The subacute form represents an altered host–organism response and is often the result of antibiotics given for other infections or nonspecific febrile illnesses. Chronic osteomyelitis, in contrast, is primarily a disease of adult life and usually develops as a result of an open wound, either traumatic or surgical.

The most common site of acute osteomyelitis in childhood is the metaphyseal end of a single long bone, frequently near the knee joint. The route of infection is usually hematogenous, although local direct extension from a neighboring soft tissue infection occasionally occurs. A history of trauma may be elicited. A primary site of infection is only rarely found. The metaphyseal area of growing bone is most frequently involved because as enchondral ossification proceeds, the blood vessels that normally invade the growth zone are looped, and, as a result, the circulation is sluggish. This can allow a nidus of infection to become established. The metaphyses also have fewer phagocytes, which may make it more susceptible.

In patients older than 50 years of age, the spine is the most common site of infection. These patients often have a history of genitourinary disease and/or manipulation, and the onset of the infection can be insidious.

CLINICAL FEATURES

In general, acute hematogenous osteomyelitis occurs primarily in late infancy and at puberty and is often preceded by signs of systemic disease and/or general sepsis for several days. The lower extremity is most commonly affected, and a mild limp may develop. Anorexia, nausea, malaise, irritability, and fever are present, usually during the acute phase. This stage of the disease may last for several days before bone pain and local overlying inflammation appear. Fever, chills, and diaphoresis are the usual systemic complaints. Pain, bone tenderness, heat, and swelling of the soft tissue are the classic physical findings. There is often limitation of motion of an adjacent joint caused by a sympathetic effusion. (Remember: an unexplained fever with bone pain in the child is osteomyelitis until proven otherwise.)

In infants, the disease may be alarming and life-threatening in its onset. The involved area usually shows limitation of motion (pseudoparalysis), and there may be tenderness in the involved bone well before swelling and redness occur.

In the adult, the onset is usually less acute. Constitutional symptoms may be considerably less marked or even absent. In the older child and the adult, it is not uncommon for the first symptoms of osteomyelitis to be those of bone involvement. Usually, there is limitation of joint motion, especially if the osteomyelitis involves the spine or if the primary lesions are particularly close to joints where sympathetic effusions may occur.

Tuberculous, fungal, and rickettsial causes of osteomyelitis generally have an insidious onset. These diseases are more common in patients who are immunologically depressed, who have other underlying diseases, such as alcoholism, or those whose immune systems have been altered by immunosuppressive therapy or human immunodeficiency virus. The primary source of these infections is often pulmonary, and a low-grade fever, weight loss, anorexia, and chronic cough or sputum production may be present. Tuberculous osteomyelitis may involve the vertebral column with pathologic fractures of the involved vertebrae. This usually results in angular kyphosis of the spine or so-called Pott’s disease (Fig. 13-1).

In the drug-abusing patient who is afebrile and presents with an onset of back pain that is aggravated by moving, coughing, sneezing, or straining at stool, pyogenic spondylitis and gram-negative osteomyelitis should be suspected.

ROENTGENOGRAPHIC FEATURES

The classic roentgenographic finding of acute osteomyelitis in childhood is deep, circumferential soft tissue swelling with obliteration of muscular planes. Spotty rarefactions representing early destruction may appear within 7 to 12 days in the affected bone. Shortly after this, periosteal new bone formation becomes evident and indicates that the infection has spread through the cortex (Fig. 13-2). Plain roentgenograms are of less value in adult osteomyelitis because significant bony changes may not be apparent until at least 50% of bone destruction has occurred, which may be 2 to 4 weeks into the illness. In the spine, infection can involve the vertebral body or the disc space. Disc space infections are uncommon but do occur occasionally in children and in patients who have undergone surgery on the intervertebral disc. In these cases, the roentgenographic changes are vertebral end-plate irregularities and disc space narrowing. Eventually, new bone proliferation occurs, and frequently complete fusion of the disc is the result. In osteomyelitis of the vertebral body, the roentgenographic changes are those of bone destruction with loss of vertebral height. Paravertebral swelling and/or paraspinal masses may also be occasionally demonstrated.

Radioisotope bone scans, usually using technetium, are a mainstay in the early diagnosis of acute osteomyelitis, although any abnormal findings are nonspecific. An advantage of the technetium scan is that it can be performed within a few hours. An isotope-labeled white blood cell (WBC) scan is more specific for infection, although this study is not always available at all facilities.

Magnetic resonance imaging (MRI) and computed tomographic (CT) scanning are also extremely valuable. MRI is more likely to be of assistance in detecting subtle changes, especially those involving the bone marrow and is the best modality for the diagnosis of acute osteomyelitis. Computed tomography can often define early soft tissue changes.

Chronic Osteomyelitis

This disorder can occasionally be the end result of an acute hematogenous osteomyelitis, but it is more commonly caused by an open fracture or wound and rarely by a surgical procedure. It is often seen in the lower extremities of patients with diabetes. All forms of chronic osteomyelitis are difficult to eradicate. The cause is often polymicrobial.

COMPLICATIONS

The most common complications of acute osteomyelitis are soft tissue abscess formation, septic arthritis from extension to the adjacent joints, and metastatic infections from the initial focus. Occasionally, chronic osteomyelitis can be a complication of acute osteomyelitis. However, this is relatively uncommon in children, because the bone of growing children is a more active substance and has the ability to “turn over” and clear itself of infection. Overgrowth of bone because of stimulation and shortening caused by growth plate destruction can also occur in the young.

The problem most often seen as a result of chronic osteomyelitis is recurrent episodes of inflammation and drainage, or even simply chronic drainage. If this occurs after the insertion of an orthopedic implant, it is often necessary to remove the orthopedic implant before the infection will subside. In weight-bearing joints, this often results in less than optimal function, but removal of the foreign body does increase the chances of curing the infection.

Development of a chronically draining sinus can also be debilitating because of the extensive protein loss through the sinus tract. On rare occasions, squamous cell carcinoma can even develop at the drainage site. Amputation is even occasionally necessary in patients with diabetes or other individuals with poor local tissue health. Extensive spinal involvement may lead to paraplegia, and pathologic fractures may even occur in weight-bearing bones.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis includes: (1) acute suppurative arthritis, (2) rheumatic fever, (3) cellulitis, and (4) tumor. The most common cause of acute septic arthritis in young adults is Neisseria gonorrhoeae, whereas S. aureus is the major nongonoccal pathogen in older adults. Also, in the older population septic arthritis is often superimposed on some other bone disease, most commonly rheumatoid arthritis. In general, the clinical manifestations of septic arthritis are variable and related to the type of organism causing the underlying infection. Most patients with gonococcal septic arthritis have prominent prodromal symptoms such as fever, chills, headaches, anorexia, and malaise, followed by the development of monoarticular septic arthritis. In gonococcal arthritis, an important portion of the diagnosis lies in the history of a migratory polyarthralgia. A tenosynovitis may be present, but cultures from this involved synovium are usually sterile; however, the skin lesions and small joint effusions are generally positive for the offending organism. The arthritis seen in gonococcal disease is that of involvement of the large joints, primarily the knee, followed by the wrists, ankles, and elbows.

The clinical picture of patients with acute rheumatic fever, gout, and rheumatoid arthritis may mimic that seen in acute septic arthritis. Synovial fluid examination is helpful. The diagnosis of acute rheumatic fever is based on Jones’ criteria of major and minor manifestations (Table 13-1).

Table 13-1 Modified Jones Criteria (Revised)

Major Manifestations
Carditis
Polyarthritis
Chorea
Erythema marginatum
Subcutaneous nodules
Minor Manifestations
Arthralgia
Fever
Prolonged PR interval
Elevated ESR, C-reactive protein
Supporting evidence of previous group A streptococcal infection
• Positive throat culture or rapid streptococcal antigen test
• Elevated or rising streptococcal antibody titer
NOTE: The presence of two major or one major and two minor manifestations indicates a high probability of acute rheumatic fever if supported by evidence of preceding group A streptococcal infection.

Cellulitis may sometimes be difficult to differentiate from septic tissue swelling on roentgenographic examination. The soft tissue swelling is primarily superficial, usually involving skin and subcutaneous tissue. The offending oranism is usually hemolytic streptococcus. Occasionally, the cellulitis can evoke a sympathetic effusion in an adjacent joint, but passive and active movements of that joint are generally not as painful as they are in acute septic arthritis. In addition, the clinical response to treatment is usually dramatic. If there is a sympathetic effusion in an adjacent joint and there is a problem in differentiation among cellulitis, septic arthritis, and acute osteomyelitis, the joint may be aspirated through an area of healthy skin, but great care must be taken to avoid contaminating a normal joint. MRI is useful is distinguishing cellulitis from osteomyelitis. The condition is commonly confused with vascular disorders in the lower leg. The tumor goes away with elevation if it is caused by peripheral vascular disease, but not if cellulitis is present.

To establish the diagnosis of tumor, special roentgenographic studies and biopsy are necessary. The rule of culturing all biopsies and taking biopsies of all cultures is always followed.

TREATMENT AND PROGNOSIS

After proper cultures are obtained, the treatment of acute osteomyelitis should begin immediately and not be delayed while waiting for the identification of the offending organism. Because the majority of cases in the young are caused by S. aureus, it is appropriate to use an IV antibiotic to cover this pathogen as well as group B streptococcus, enteric rods, and probably H. influenza as well. In addition to the proper antibiotic coverage, the patient should have general supportive measures. Dehydration and anemia should be corrected, and the diet should be high in vitamins and protein. Early surgical drainage and debridement are indicated in acute osteomyelitis unless there has been a rapid clinical response within 24 to 36 hours. The extremity should be properly immobilized for a period of 3 to 4 weeks.

If necessary, changes are made in the antibiotic coverage when the offending organism is identified. The sedimentation rate and C-reactive protein levels are followed during treatment. IV antibiotic coverage is usually continued for 4 weeks, but each case should be treated individually, and there is no consensus regarding the route and length of antibiotic coverage. Treatment for the subacute form is essentially the same.

Sometimes fever may recur after an initially good response to the appropriate antibiotic treatment. At this time, a careful clinical reevaluation is necessary, and several conditions should be considered: (1) laboratory error in identification of the organism, (2) drug fever (usually due to a cephalosporin or a penicillin), (3) superinfection, (4) abscess formation, or (5) inadequate drainage.

In general, the prognosis for acute osteomyelitis is good, although complications have been reported in as many as 25% of cases. If antibiotic treatment is begun before bone and tissue necrosis has occurred, surgery is less often required. A delay in diagnosis and treatment may lead to chronic osteomyelitis or multiple recurrences. These recurrences can develop as long 30 years later and are usually caused by the same organism. They are often reactivated by minor local trauma.

The treatment of chronic osteomyelitis is similar to that of the acute form, but prevention remains the most important aspect of this disease. All open fractures are meticulously cleaned and debrided, and great care is taken to eliminate contamination. Once chronic osteomyelitis develops, it may be treated by incision and drainage, radical debridement, and appropriate antibiotic coverage for 4 to 6 weeks. However, once it is established, chronic osteomyelitis is difficult to cure. Recurrent drainage and residual deformity both add to the morbidity. Local infection that develops in the presence of a prosthetic device may necessitate removal of the device before the infection can be controlled.

Infections of the bones of the feet are common in diabetic patients, who often have coincidental peripheral vascular disease. Painless ulcers may develop secondary to diabetic polyneuropathy and diabetic vascular disease. Hyperemia and swelling are frequently noted clinically. If a fracture occurs in the foot of a diabetic patient, it may be accompanied by a similar redness and swelling and be a source of some confusion. A roentgenogram usually clarifies the diagnosis.

Septic Arthritis

Septic arthritis may occur in any age group but is more common in the young. It is usually monoarticular, and large peripheral joints are most frequently involved, usually the knee or hip. Polyarticular disease is rare but may occur in patients with preexisting inflammatory disease or chronic illness. Unusual sites (sacroiliac, sternoclavicular joints, and symphysis pubis) may be involved in IV drug abusers. The etiology of most cases is bacterial, although viral and even fungal causes have been demonstrated.

Gonococcal infection often leads to a distinct clinical syndrome and is discussed separately.

Special Problems

CELLULITIS

Cellulitis is a common diffuse spreading superficial infection of the skin and subcutaneous tissue. It may arise from a break in the skin (often from a skin fissure between the toes) or a surgical wound, although in most patients no obvious cause is found. It is more common in diabetic patients and patients with lymphatic or venous compromise. The deeper structures are usually not involved, and abscess formation is rare.

The offending organism is usually hemolytic streptococcus, although S. aureus, and, rarely, Gram-negative rods may be causative. The clinical presentation varies depending on the organism, but streptococcus usually causes a superficial warm, tender erythematous lesion characterized by an elevated, indurated margin. Vesicle formation may occur. Samples for Gram stain and culture may be obtained from this fluid or any local drainage. MRI may rarely be needed to determine the extent of soft tissue involvement and to rule out bony involvement.

Treatment consists of elevation, rest (with immobilization, if needed), and the appropriate antibiotic. The oral route is often sufficient, but intravenous antibiotics may be needed in more severe cases. Surgery is generally not required unless an abscess develops. The prognosis is usually good.

Cellulitis may be mistaken for vascular disease in the lower leg. As a rule, the rubor associated with vascular insufficiency goes away with elevation but not if due to infection. Chronic venous stasis can also be a source of confusion, and the two conditions may occasionally coexist.

NOTE: If cellulitis develops near a joint, a reactive, sterile effusion may develop in that joint. Care must be taken to differentiate cellulitis from a joint infection. If a needle is passed through the soft tissue infection and into the joint in the process of analyzing the effusion, sepsis can be introduced, creating a pyogenic joint infection.

GAS GANGRENE

Clostridia organisms are widely distributed in nature, but only a few are severe pathogens. Several species can cause gas gangrene in humans. The most common is Clostridium perfringens (C. welchii). Other causes are C. novyi, C. histolyticum, C. septicum, C. bifermentans, and C. fallax.

Gas gangrene is an uncommon clinical infection in which a severe soft tissue wound or surgical trauma allows the tissue to become contaminated with the Clostridium spore. Local anaerobic conditions (a closed wound) favor conversion from the spore form to the vegetative form, which produces the potent toxins typical of this disorder. These toxins destroy soft tissue and muscle and can cause severe septic shock and death. Other organisms, including group A β-hemolytic streptococcus, may cause necrotizing soft tissue infections.

SEPTIC BURSITIS

Infection of superficial bursae is a common occurrence. The bunion, olecranon, and prepatellar bursae are the most commonly affected. In contrast to septic arthritis, this disorder usually occurs in healthy individuals and commonly results from local spread. Occupations that predispose to chronic trauma and fluid collection in the bursa (e.g., carpet layers, plumbers) are more prone to sepsis in this area. There may be evidence of a recent local abrasion or break in the skin. S. aureus is the most common offending organism.

PENETRATING WOUNDS

GUNSHOT WOUNDS

The amount of damage done to tissues by gunshot wounds depends on the velocity of the weapon. Low-velocity weapons usually cause minimal wound tract injury. Important structures are usually pushed away by the missile. These injuries are best treated on an outpatient basis by minimal local debridement of the entrance (and exit) wound, irrigation, a sterile dressing, and a broad-spectrum antibiotic. Tetanus prophylaxis is administered, and if necessary, delayed closure is performed later. Associated fractures are usually undisplaced and are treated by external immobilization.

Bullet removal or operative exploration is undertaken only if the bullet is superficial or symptomatic or if minor fragment migration could cause damage to major adjacent structures. Missile wounds of the knee joint probably should be explored surgically and debrided if fragments are present or if the joint was traversed. The missile and osteochondral fragments are removed. It is possible for lead to be dissolved by synovial tissue and lead to arthritis (lead arthropathy) and, rarely, chronic lead intoxication. Factors involved in systemic lead intoxication include the surface area and amount of fragmentation of the bullet, as well as duration of exposure. Elsewhere in the body, the fragments are usually encapsulated by scar tissue, thereby eliminating their exposure to bodily fluids. Fragments near the spine are usually left alone unless a significant or progressive neural loss occurs.

Wounds caused by high-velocity weapons are managed the same way as those caused by low-velocity weapons, except that more extensive debridement is usually necessary. Their complication rate is much higher, and delayed closure is the rule.

Shotgun wounds also require more extensive debridement. They are often the most serious of missile wounds. The projectile consists of multiple pellets and a wadding (usually fiber or burlap) that transmits the force. Wounds inflicted from a weapon closer than 20 yards are assumed to contain some of this wadding, and exploration and removal are necessary. If the “scatter pattern” of the shotgun is wide, more damage is assumed, especially if the shotgun was fired at close range. A small wound can disguise extensive deeper destruction.

BITE WOUNDS

More than 1% of all emergency room visits are the result of bites, and the majority of these wounds are superficial. Dog bites account for most of these wounds. They usually present as small puncture wounds. The infection rate is low, and very loose closure of any extensive wound is usually acceptable after thorough cleansing, irrigation, and debridement. Extremity wounds may be left open; however, small puncture wounds should not be opened. Prophylactic antibiotic therapy is indicated, using an agent with activity against S. aureus, β-hemolytic streptococci, anaerobic streptococci, and Pasturella multocida, which is a frequent cause of infection after dog and cat bites. Antirabies therapy and tetanus prophylaxis are provided when indicated.

Human bites require especially careful evaluation and examination. The most common site of injury is a closed fist that has struck the mouth (see Chapter 7). The injury that often occurs is a laceration over the metacarpophalangeal joint that may disrupt the extensor tendon and even penetrate into bone (Fig. 13-6). The wound may be small, and if the hand is examined with the fingers extended, the true extent of the injury may be overlooked because the injury was sustained with the fingers flexed. If joint involvement is noted, extra care is taken to ensure good cleansing and debridement. The wound should be treated open. Antibiotics are administered, and the wound is followed closely. The most common infecting organisms are S. aureus, streptococci, and anaerobes found in the normal flora of the human mouth. In addition, prophylactic therapy is indicated for those who are bitten by individuals with HIV or hepatitis B.

BIBLIOGRAPHY

Altemeier WA, Fullen WD. Prevention and treatment of gas gangrene. JAMA. 1971;217:806-813.

Ashby ME. Low-velocity gunshot wounds involving the knee joint: surgical management. J Bone Joint Surg Am. 1974;56:1047-1053.

Bartlett CS, Helfet DL, Hausman MR, et al. Ballistics and gunshot wounds: effects on musculoskeletal tissues. J Am Acad Orthop Surg. 2000;8:21-36.

Boll KL, Jurik AG. Sternal osteomyelitis in drug addicts. J Bone Joint Surg Br. 1990;72:328-329.

Brettler D, Sedlin ED, Mendes DG, et al. Conservative management of low velocity gunshot wounds. Clin Orthop Relat Res. 1979;140:26-31.

Brown PW, Kinman PB. Gas gangrene in a metropolitan community. J Bone Joint Surg Am. 1982;56:1445-1451.

Chuinard RG, D’Ambrosia RD. Human bite infections of the hand. J Bone Joint Surg Am. 1977;59:416-418.

Dich VQ, Nelson JD, Haltalin KC. Osteomyelitis in infants and children. Am J Dis Child. 1975;129:1273-1278.

Dormans JP, Drummond DS. Pediatric hematogenous osteomyelitis: new trends in prevention, diagnosis, and treatment. J Am Acad Orthop Surg. 1994;2:333-341.

Edson RS, Terrell CL. The aminoglycosides. Mayo Clin Proc. 1991;66:1158-1164.

Eismont FJ, Bohlman HH, Soni PL, et al. Pyogenic and fungal vertebral osteomyelitis with paralysis. J Bone Joint Surg Am. 1983;65:19-29.

Eismont FJ, Bohlman HH, Soni PL, et al. Vertebral osteomyelitis in infants. J Bone Joint Surg Br. 1982;64:32-35.

Emmons CW, Binford CH, Utz JP. Medical mycology, ed 2, Philadelphia: Lea & Febiger, 1970.

Freij BJ, Kusmiesz H, Shelton S, et al. Imipenem and cilastatin in acute osteomyelitis and suppurative arthritis. Therapy in infants and children. Am J Dis Child. 1987;141:335-342.

Gentry LO. Overview of osteomyelitis. Orthop Rev. 1987;16:255-258.

Green M, Nyhan WLJr, Fousek MD. Acute hematogenous osteomyelitis. Pediatrics. 1956;16:368-382.

Guidelines for the diagnosis of rheumatic fever 1992 Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 Update. JAMA. 1992;268:2069-2073.

Gustaferro CA, Steckelberg JM. Cephalosporin antimicrobial agents and related compounds. Mayo Clin Proc. 1991;66:1064-1073.

Hart GB, O’Reilly RR, Cave RH, et al. The treatment of clostridial myonecrosis with hyperbaric oxygen. J Trauma. 1974;14:712-715.

Hoeprich PD. Infectious diseases. Hagerstown, Md: Harper & Row, 1972.

Holzman RS, Bishko F. Osteomyelitis in heroin addicts. Ann Intern Med. 1971;75:693-696.

Hughes SPF, Fitzgerald RHJr. Musculoskeletal infections. Chicago: Year Book Medical Publishers Inc, 1986.

JONES criteria (modified) for guidance in diagnosis of rheumatic fever 1955 JONES criteria (modified) for guidance in diagnosis of rheumatic fever. Mod Concepts Cardiovasc Dis. 1995;24:191-193.

Kocher MS, Mandiga R, Murphy JM, et al. A clinical practice guideline for treatment of septic arthritis in children: efficacy in improving process of care and effect on outcome of septic arthritis of the hip. J Bone Joint Surg Am. 2003;85-A:994-999.

LaMont RL, Anderson PA, Dajani AS, et al. Acute hematogenous osteomyelitis in children. J Pediatr Orthop. 1987;7:579-583.

Lazzarini L, Mader JT, Calhoun JH. Osteomyelitis in long bones. J Bone Joint Surg Am. 2004;86-A:2305-2318.

Lifeso RM, Rooney RJ, el-Shaker Ml. Post-traumatic squamous cell carcinoma. J Bone Joint Surg Am. 1990;72:12-18.

May JWJr, Jupiter JB, Weiland AJ, et al. Clinical classification of post-traumatic tibial osteomyelitis. J Bone Joint Surg Am. 1989;71:1422-1428.

McCarthy JJ, Dormans JP, Kozin SH, et al. Musculoskeletal infections in children. Basic treatment principles and recent advancements. J Bone Joint Surg Am. 2004;86A:850-863.

Nade S. Septic arthritis. Best Pract Res Clin Rheumatol. 2003;17:183-200.

Ortiz E, Sande MA. Routine use of anaerobic blood cultures: are they still indicated? Am J Med. 2000;108:445-447.

Ouzounian TJ, Thompson L, Grogan TJ, et al. Evaluation of musculoskeletal sepsis with indium-111 white blood cell imaging. Clin Orthop Relat Res. 1987;221:304-311.

Patzakis MJ, Zalavras CG. Chronic posttraumatic osteomyelitis and infected nonunion of the tibia: current management concepts. J Am Acad Orthop Surg. 2005;13:417-427.

Presutti RJ. Prevention and treatment of dog bites. Am Fam Physician. 2001;63:1567-1572.

Schmid FR. Principles of diagnosis and treatment of infectious arthritis. In Hollander JL, McCarty DJJr, editors: Arthritis and allied conditions, ed 8, Philadelphia: Lea & Febiger, 1972.

Sokolowski MJ, Sisson GJr. Systemic lead poisoning due to an intra-articular bullet. Orthopedics. 2005;28:411-412.

Song KM, Sloboda JF. Acute hematogenous osteomyelitis in children. J Am Acad Orthop Surg. 2001;9:166-175.

Smith DL, McAfee JH, Lucas LM, et al. Septic and nonseptic olecranon bursitis. Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med. 1989;149:1581-1585.

Stulberg DL, Penrod MA, Blatny RA. Common bacterial skin infections. Am Fam Physician. 2002;66:119-124.

Sucato DJ, Schwend RM, Gillespie R. Septic arthritis of the hip in children. J Am Acad Orthop Surg. 1997;5:249-260.

Tay BK, Deckey J, Hu SS. Spinal infections. J Am Acad Orthop Surg. 2002;10:188-197.

Thompson GR, Ferreya A, Bracket RG. Acute arthritis complicating rubella vaccinations. Arthritis Rheum. 1971;14:19-26.

Thompson RL, Wright AJ. Cephalosporin antibiotics. May Clin Proc. 1983;58:79-87.

Waxman AD, Bryan D, Siemsen JK. Bone scanning in the drug abuse patient: early detection of hematogenous osteomyelitis. J Nucl Med. 1973;14:647-650.

Wilkowske CJ, Hermans PE. General principles of antimicrobial therapy. Mayo Clin Proc. 1987;62:789-798.

Wright AJ, Wilkowske CJ. The penicillins. Mayo Clin Proc. 1987;62:806-820.

Wright AJ, Wilkowski CJ. The penicillins. Mayo Clin Proc. 1991;66:1047-1063.

Yeargan SA3rd, Perry JJ, Kane TJ3rd, et al. Hematogenous septic arthritis of the adult hip. Orthopedics. 2003;26:771-776.

Yuh WT, Corson JD, Daraniewski M, et al. Osteomyelitis of the foot in diabetic patients: evaluation with plain films, 99 Tc-MDP bone scintigraphy and MR imaging. AJR Am J Roentgenol. 1989;152:795-800.