Infectious arthritis is defined as infection of one or more joints. It can be caused by bacteria, fungi, viruses, and parasites.
Acute Bacterial Arthritis
Native joint septic arthritis is an uncommon illness, with a reported incidence in the United States of 2 to 10 cases per 100,000 persons per year. However, the incidence appears to be rising, in part due to an increasing number of joint surgical procedures performed in the United States and because of a larger “at-risk population.” The incidence of septic arthritis is higher in certain at-risk groups, including patients with rheumatoid arthritis and patients with a low socioeconomic status. Bacterial septic arthritis accounts for 8% to 27% of patients presenting with one or more acutely painful joints in the emergency room (ER). The knee joint is the most commonly affected joint. Septic arthritis is associated with significant morbidity; near half of the patients report decreased joint mobility after the infection. This, however, also depends on previous underlying joint disease and the type of microorganism involved. Bacterial arthritis is generally acquired hematogenously. Underlying joint architectural abnormality increases the risk of pyogenic arthritis. An important factor to consider is that the synovial membrane is a highly vascularized structure that lacks a basement membrane and is susceptible to hematogenous deposition of bacteria. Other routes of infection include trauma; animal bites; joint puncture from a nail, needle, or thorn; iatrogenic infection; and contiguous infection from adjacent soft tissue or bone. After knee arthroscopy, the infection risk is 0.04% to 0.4%, and after arthroscopic reconstruction, the risk is 0.14% to 1.7%. Rarely, septic arthritis has occurred in clusters after intraarticular injection of contaminated methylprednisolone.
Penetrating joint trauma
Intravenous (IV) drug use
Crystal-induced arthritis (gout and pseudogout), osteoarthritis, and Charcot arthropathy
Chronic systemic diseases, including collagen vascular diseases, malignancy, chronic liver disease, sickle cell disease, and alcoholism
Low socioeconomic status
Underlying joint disease especially due to rheumatoid arthritis is an important risk factor. Additionally, being treated with immunosuppressive medications such as penicillamine, sulfasalazine, anti–tumor necrosis factor alpha (anti-TNF) agents (doubles the risk according to one study), and corticosteroids further increase the risk. HIV infection, however, has not been associated with septic arthritis. In many cases, no predisposing risk factor is isolated.
Adherence of bacteria to the synovial membrane followed by colonization and replication in synovial fluid is then followed by production of inflammatory cytokines and modulators. Bacteria such as Staphylococcus aureus have cell surface receptors that bind to joint extracellular matrix, promoting invasion. Joint damage results both directly from bacterial toxins and the host inflammatory response. Purulence is observed as a result of accumulation of acute and chronic inflammatory cells. This leads to destruction of joint cartilage. Joint effusion also leads to raised intraarticular pressure predisposing to decreased blood flow and tissue necrosis. Eventually, a joint space becomes narrow, and erosion of bone and cartilage occurs if arthritis is untreated.
In adults, Gram-positive cocci such as S. aureus or streptococci are responsible for the majority of native arthritis. S. aureus is responsible for 37% to 65% of the cases, with a higher incidence in patients with underlying rheumatoid arthritis.
Methicillin-resistant S. aureus (MRSA) is seen in elderly, those with recent orthopedic surgery, and those who are colonized with MRSA. Of the streptococci, Streptococcus agalactiae is a cause of bacterial arthritis in neonates, adults with malignancy, diabetes, and urogenital anatomic abnormalities and predisposes to polyarticular infection. Streptococcus bovis subgroup gallolyticus septic arthritis could be a manifestation of infective endocarditis; thus these patients should be evaluated for endocarditis and colonic malignancy.
Gram-negative rods account for 9% to 17% of all cases, and anaerobes are identified in 1% to 3%. Again, elderly and immunocompromised patients and IV drug users are at a higher risk. Pseudomonas aeruginosa is seen frequently in IV drug users and is also recognized as a cause of iatrogenic septic arthritis. In young infants, Haemophilus influenzae has now been replaced by Kingella kingae , a resident of oral flora.
Zoonotic pathogens such as Pasteurella multocida and Capnocytophaga spp. can occasionally cause contiguous septic arthritis after a dog or cat bite. Streptobacillius moniliformis , the cause of rat bite fever, can cause polyarticular arthritis after a rat bite. Cases of bacterial arthritis where a pathogen is not isolated from blood or joint fluid using conventional culture techniques are Mycoplasma hominis, Ureaplasma urealyticum, Borrelia burgdorferi and Tropheryma whipplei.
The knee is the most common joint involved in nongonococcal septic arthritis followed by the hip, shoulder, wrist, and ankle. Arthritis of the small joints of the foot are seen generally in diabetics with adjacent skin and soft tissue ulceration. Polyarticular presentation may be seen in patients who are immunosuppressed (such as patients with rheumatoid arthritis [RA]) or patients with high-grade bacteremia (especially with S. aureus ). In cases of S. aureus bacteremia, sacroiliitis can also be seen.
The typical presentation is one of progressive pain, loss of function, and loss of range of motion of the involved joint seen over a period of several days, up to 2 weeks, depending on the organism and patient. Other symptoms include joint swelling, redness, and warmth. Fever and malaise can also be seen, though high-grade fever with rigors is rare, unless accompanied by bloodstream infection. Physical examination typically demonstrates joint tenderness, effusion and limitation of active and passive range of motion, and painful weight bearing. However, in older and immunocompromised patients, these symptoms may be subtle, leading to a delay in diagnosis.
There is no single laboratory finding that is sensitive or specific for native septic arthritis. Leukocytosis, elevated erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) are helpful when present.
Synovial Fluid Analysis/Microbiologic Diagnosis
Aspiration of the joint space will often yield synovial fluid that is low viscosity and purulent. Synovial fluid white blood cell (WBC) count is typically 50,000 cells/mm 3 with a neutrophilic predominance, although lower counts are regularly seen and should not be ignored. Gram staining lacks sensitivity for the diagnosis of septic arthritis and is only diagnostic in 50% of cases. On the other hand, among patients who have not received prior antibiotics, synovial fluid culture will yield bacterial growth more than 60% of the time in nongonococcal infection. Blood cultures should always be drawn, as they can be positive in 50% of the cases. The synovial fluid broad-range polymerase chain reaction (PCR) test holds promise but is not available in all clinical microbiology labs. It is particularly useful in cases of slow-growing microorganisms such as K. kingae, Coxiella burnetii, Bartonella henselae, and Mycobacterium tuberculosis . It can be helpful in situations where patients have already received systemic antibiotics.
Early in the course of bacterial arthritis, plain radiography will show periarticular soft tissue swelling, but the bony structures are normal. Later, as the infection progresses, loss of joint space, periosteal reaction, periarticular osteoporosis, and subchondral bone destruction can be seen. Plain films help rule out the presence of any foreign body.
Ultrasound is another technique that can be used to assess for the presence of effusion and for assistance in joint aspiration. Computed tomography (CT) scan and magnetic resonance imaging (MRI) are additional and sensitive imaging modalities, especially in detecting early septic arthritis, as well as detecting periarticular fistulas, abscesses, and adjacent/periarticular cellulitis and tenosynovitis.
Native septic arthritis due to infection with Neisseria gonorrhoeae results from a complication of mucosal gonococcal infection. Risk factors associated with gonococcal arthritis are similar to those for genital gonococcal infection, including low socioeconomic status, men who have sex with men, illicit drug use, and having multiple sexual partners.
After mucosal inflammation and infection with N. gonorrhoeae , occult bacteremia results. Mucosal infection may be asymptomatic. Bacteremia can result in wide dissemination from the infected mucosa, resulting in several joints being involved (disseminated gonococcal infection). N. gonorrhoeae possesses several virulence factors that help in its attachment to the mucosal and synovial membranes, including a long pili. The pili also prevents it from undergoing host leukocyte phagocytosis.
Generally, disseminated gonococcal infection is characterized by a triad of dermatitis, tenosynovitis, and a migratory polyarthralgia/polyarthritis. Patients present with fever, chills, and malaise, with painful tenosynovitis of fingers and hands and occasionally lower limb joints. Less than half of the patients will have true septic joint effusion. A rash involves the palms and soles and can range from macules to papules and a pustular rash as well. Isolated septic gonococcal arthritis without accompanying tendinopathy and skin manifestations is less common, with knees, wrists, and ankles being most commonly affected. This is characterized by an inflamed and swollen joint with an effusion.
ESR is raised in half of the patients, accompanied by mild leukocytosis. Joint aspiration reveals a pyogenic aspirate, with WBC count ranging from 50,000 to 100,000 WBCs/mm 3 (mainly neutrophils), but lower cell counts are seen in patients with disseminated gonococcal infection with less intense pyogenic process. Gram stain of the joint aspirate reveals intracellular and extracellular Gram-negative diplococci in 25% of the cases. PCR assay of the synovial fluid is another technique for detecting the presence of N. gonorrhoeae. It is also reasonable to perform mucosal swabs and send them for culture, as recovery of N. gonorrhoeae from the mucosal sites is higher than from synovial fluid or blood cultures. Nucleic acid amplification tests (NAATs) can also be performed on urine and swabs from cervical or urethral swabs.
It is important to differentiate bacterial arthritis from noninfectious causes. Situations such as an acute attack of gout, pseudogout, and other crystalline joint arthropathies can mimic acute bacterial arthritis, as symptoms and signs can overlap.
Presence of crystals in joint fluid does not rule out bacterial arthritis. Gram stain and culture along with cell count with differential should be performed on all joint aspirates. Recognition of bacterial arthritis in patients with underlying rheumatoid arthritis is important as well. Gonococcal arthritis (when it presents as part of disseminated gonococcal infection [DGI]) should be differentiated from reactive arthritis, which is typically seen after a recent gastrointestinal or genitourinary infection. The typical rash of DGI is not seen in reactive arthritis; these patients generally have concurrent sacroiliitis, conjunctivitis, and penile manifestations such as circinate balanitis and keratoderma blennorrhagica.
Acute septic arthritis requires prompt joint drainage and is an infectious diseases emergency. Whether it requires arthroscopy or open arthrotomy depends on the clinical situation and on the surgeon. Another approach is to drain the joint through daily closed needle aspiration until clinical improvement is seen. For bacterial infections involving the knee, shoulder, and wrist, arthroscopy is preferred; however, open arthrotomy is often required for the management of septic arthritis of the hip joint. In the published literature, there are no significant differences in the outcome between arthroscopy and arthrotomy for the initial drainage of the knee, hip, and other joints.
If infection has already destroyed the articular surface and underlying bone, then resection of the infected area is considered as well. In a case of severe hip septic arthritis, this would mean resection of the femoral head (Girdlestone procedure). Alternatively, arthrodesis may be performed, in which surgical fusion of the bones across former synovial space occurs, typically performed after septic arthritis of the knee or ankle. Amputation is indicated only in overwhelming and life-threatening infections or persistent local infection with significant bone loss, where the functional benefit after amputation is superior to limb salvage.
Along with joint drainage, concomitant antimicrobial therapy is must ( Table 13.1 ). In general, parenteral therapy or use of highly bioavailable therapy is preferred over the use of other oral agents. Whether or not Gram stain reveals Gram-positive cocci, given increasing prevalence of health care–associated MRSA and community acquired (CA)–MRSA, vancomycin should be included in the initial empirical therapy. If the Gram stain is noted for Gram-negative rods (or if Gram-negative organisms are suspected), then patients should also be started on an antipseudomonal cephalosporin. If specific epidemiologic or clinical factors raise concern for β-lactamase–producing pathogens, then a carbapenem antibiotic is indicated. If methicillin-susceptible S. aureus is identified, vancomycin can be de-escalated to an antistaphylococcal penicillin such as nafcillin or a first-generation cephalosporin such as cefazolin. Alternatives to vancomycin for MRSA septic arthritis include daptomycin, ceftaroline, and linezolid. These alternatives are used when a patient has an allergy or is intolerant to vancomycin. If vancomycin-resistant Enterococcus is recovered in cultures, then daptomycin or linezolid may be used. Adverse effects of daptomycin include muscular toxicity, evident by elevated creatine kinase or, rarely, eosinophilic pneumonia. Linezolid inhibits ribosomal proteins and can be given intravenously or orally at equivalent doses. Adverse effects of linezolid include peripheral or optic neuropathy, anemia, thrombocytopenia, and lactic acidosis. Other drugs with Gram-positive activity include tigecycline, ceftaroline, trimethoprim/sulfamethoxazole, and doxycycline or minocycline. In cases of septic arthritis due to human or animal bites, ampicillin–sulbactam or amoxicillin–clavulanate are preferred due to their activity against oral anaerobes. In cases of gonococcal arthritis, ceftriaxone 1 g IV daily is preferred. Fluoroquinolones are also used due to their Gram-negative spectrum. In all situations, definitive therapy should be chosen based on the antimicrobial susceptibility testing, with input based on cost and adverse effects, individualized to the patient.
|Microorganisms||Treatment of Choice (IV)||Alternatives (IV)|
|Gram-positive cocci||Vancomycin||Daptomycin a|
|Cefazolin, nafcillin, or oxacillin||Ceftriaxone or vancomycin b|
|Methicillin-resistant S. aureus||Vancomycin||Daptomycin or teicoplanin (where available)|
|Streptococcus spp.||Penicillin G||Ceftriaxone or vancomycin b|
|Gram-negative rods||Ceftriaxone or ceftazidime or cefepime c||Ciprofloxacin or levofloxacin or carbapenem|
|Enterococci||Ampicillin, penicillin G||Vancomycin or daptomycin|
|Gram-stain negative (but cell count consistent with septic arthritis)||Vancomycin a plus cefepime or ceftazidime||Daptomycin a plus piperacillin–tazobactam or fluoroquinolone or carbapenem|
There is a lack of consensus with regard to the optimal duration of therapy for septic arthritis. Generally, 2 weeks IV therapy for streptococci, 3 to 4 weeks IV therapy for staphylococci and Gram-negative bacteria, and greater than 4 weeks may be needed for immunocompromised patients and other host comorbidities such as extent of joint damage. For gonococcal arthritis, 7 to 14 days of therapy with ceftriaxone is the standard.
Generally, fungal arthritis affects immunocompromised patients, such as patients with RA or inflammatory bowel disease who are on high-dose corticosteroids or TNF-alpha inhibitor therapy. Common pathogens include Candida spp., Cryptococcus spp., Aspergillus spp., and other molds. Except for Candida species, most of these fungal pathogens have primary pulmonary infection with secondary hematogenous seeding of a joint in the setting of augmentation of immunosuppression. Occasionally, healthy hosts can develop fungal arthritis; this is typically seen in endemic mycoses and include Blastomyces dermatitidis , Histoplasma capsulatum, Coccidioides spp., and Sporothrix spp.
Risk factors for candidal arthritis include diabetes, malignancy, hemodialysis, IV drug abuse, and immunosuppressive medications, as well as prolonged use of broad-spectrum antibiotics. Infection is mostly acquired hematogenously. Candida albicans is the most common species, and the knee joint is most commonly affected. Synovial fluid analysis reveals low glucose and polymorphonuclear leukocytes, typically in excess of 50,000 cells/mm 3 .
The causative organism is Cryptococcus neoformans, with arthritis typically seen concomitantly with cryptococcal osteomyelitis. The knee joint is commonly affected, and immunosuppression is the main risk factor. In addition to synovial fluid fungal cultures needed for diagnosis, serum cryptococcal antigen must be sent.
This is typically seen in the southwestern regions of the United States. Causative fungi are Coccidioides immitis and Coccidioides posadasii . Infection generally is introduced via inhalation, followed by pneumonitis and polyarticular arthritis seen in one-third of the patients. Disseminated coccidioidomycosis is seen in ≈1%. Patients typically present with chronic granulomatous infection of bones and joints. The knee joint is the most commonly affected, and many times, infection is indolent in its course. Synovial fluid has a lymphocytic predominance, and spherules can be seen as well. Serologic testing includes serum coccidioides antibody testing and is confirmed on fungal culture of synovial fluid.
This primary infection due to B. dermatitidis usually involves the pulmonary tract and can disseminate, with joint involvement seen in patients with subjacent osteomyelitis. Occasionally, draining sinus tracts are seen as well. Diagnosis is made by cytologic examination of synovial fluid and confirmed upon performing synovial fluid fungal cultures.
Fungal arthritis due to Histoplasma capsulatum is rare, but should be considered in patients from endemic areas with chronic joint infection. Arthritis due to S porothrix is generally seen in the setting of traumatic injury with a foreign body contaminated with soil. Diabetes and immunosuppression are risk factors, and diagnosis is often challenging due to synovial fluid cultures being frequently negative. Other fungal species that cause arthritis include Aspergillus , Fusarium spp., and Scedosporium spp., organisms that are typically seen in immunocompromised hosts.
Treatment of Fungal Arthritis
The surgical approach varies from case to case. Patients may need open versus arthroscopic debridement. Treatment of Candida arthritis should be based upon antifungal susceptibility testing. An echinocandin is appropriate treatment, pending susceptibility testing, but oral triazole therapy is appropriate once susceptibilities return. For the endemic mycoses ( Coccidioides, Histoplasma, Sporothrix, Blastomyces spp.), treatment is with itraconazole 200 mg twice daily for up to a year. Finally, for Aspergillus species, voriconazole is generally preferred.
Viral arthritis tends to be acute in presentation and accompanied by a systemic febrile illness.
This is the most common form of viral arthritis. It presents with a classic facial rash in children, whereas in adults, it presents with a febrile illness accompanied by polyarthralgia. It is more common in females; patients can have involvement of knees, wrists, ankles, and metacarpophalangeal and interphalangeal joints. In addition to clinical examination, diagnosis is made by positive serology and peripheral blood PCR. Treatment is with nonsteroidal antiinflammatory drugs (NSAIDs), and rarely, IV immunoglobulin is used.
Arthritis due to rubella virus can result after natural infection or after immunization with live-attenuated vaccine. It affects small joints of the hands, followed by knees, wrists, and ankles. Treatment is generally supportive and NSAIDs.
Hepatitis B and C
Both infections have been associated with an inflammatory arthritis syndrome, better described with hepatitis B. This tends to mimic RA, with a predilection for the small joints of the hand and feet. Management requires treating underlying hepatitis B and C infections along with providing supportive care.
M. tuberculosis spreads to the bones and joints hematogenously, typically from a pulmonary focus. It presents as an oligoarticular arthritis, typically affecting weight-bearing joints such as the hip, knee, and ankle but can involve any joint. Joints are generally involved from adjacent tuberculous osteomyelitis. Pathogenesis involves local inflammation that evolves into formation of granulation tissue followed by destruction of cartilage, demineralization, and bone necrosis.
In advanced stages, periarticular cold abscesses and fistulas may be seen. Although M. tuberculosis is endemic throughout countries in the developing world, in nonendemic areas, the high-risk population includes homeless people from inner cities, immigrants, persons with a substance abuse disorder, and malnourished individuals. Diagnosis of tuberculous arthritis involves, first of all, a high index of suspicion. Radiologic findings typically reveal “Phemister triad,” characterized by juxtaarticular osteoporosis, gradual narrowing of joint space, and peripherally located osseous erosions.
Synovial tissue biopsy has a yield of 90% via arthroscopic biopsy, whereas culture has a yield of 80%. M. tuberculosis grows slowly, so newer techniques involving PCR-based tests that use amplification of parts of the bacterial genome have shown promise. Treatment of tuberculous arthritis is similar to treatment of pulmonary tuberculosis and includes combination antituberculous therapy and, depending on the clinical situation, surgical debridement. Antituberculous therapy involves two phases, with an intensive bactericidal phase in which four medications are typically used, followed by 4 to 8 months of a continuation phase, typically with two medications. The first-line medications include isoniazid, streptomycin, rifampin, pyrazinamide, and ethambutol.
Nontuberculous Mycobacterial Arthritis
These infections are uncommon. Most patients have preexisting joint disease and predisposing factors, with HIV infection/AIDS historically being the most common. Infection with many of the more than 120 species of Mycobacteria has been reported. As with tuberculous septic arthritis, management includes combination antimycobacterial therapy, often in conjunction with surgical debridement.
Osteomyelitis, infection of bone, can develop hematogenously or as a result of contiguous spread from adjacent soft tissues in the setting of vascular insufficiency or neuropathy. It can also result after trauma or surgery.
The Lew and Waldvogel classification system takes into account duration of infection, route of infection (hematogenous vs. contiguous), and presence of vascular insufficiency. Acute osteomyelitis develops over days to weeks. Subacute osteomyelitis can be caused by Brucella species or M. tuberculosis or low-virulence organisms such as Cutibacterium acnes in the presence of an implant. Chronic osteomyelitis is a smoldering form of osteomyelitis characterized by dead bone and can persist for years.
Finally, as further outlined in this chapter, osteomyelitis can also be classified by location. It can involve the vertebral column (axial skeleton) or the appendicular skeleton (including long bones). In adults, the vertebral column is the most common site for hematogenous osteomyelitis, whereas the appendicular skeleton is the most common site for contiguous osteomyelitis.
Infection of the vertebral endplate and the adjacent vertebral body is often referred to as spondylodiscitis . An associated disk space infection is often also present, and an epidural or psoas abscess may or may not be present as well. The intervertebral disk is cartilaginous in origin and lacks blood supply of its own. Microorganisms arrive via arterial blood supply, invade the adjacent endplates, and then may go on to infect the disk cartilage. Hematogenous seeding can result from primary infection of skin and soft tissues, urogenital infections, infective endocarditis in IV drug users, and in patients with respiratory tract infections. Infection can also result iatrogenically, after spine surgery, via epidural injections, or spinal trauma.
Acute vertebral osteomyelitis is typically caused by S. aureus and coagulase-negative staphylococci, Streptococcus spp., and aerobic Gram-negative rods such as Escherichia coli and P. aeruginosa. Candida species can also cause osteomyelitis, which is often diagnosed late; typically patients are IV drug users or immunosuppressed patients. Subacute and chronic vertebral osteomyelitis are caused by M. tuberculosis and Brucella species and are seen in regions endemic for those organisms or among patients with suggestive exposure history. Osteomyelitis due to viridans group streptococci has a subacute presentation as well and occurs in the setting of endocarditis. Spinal hardware–associated osteomyelitis can be caused by S. aureus (which typically occurs within 30 days of surgery) or can also be caused by coagulase-negative staphylococci or C. acnes .
Patients present with localized back pain and tenderness. Fever is seen in only half of the patients. The lumbar spine is the most frequently affected anatomic region, followed by the thoracic spine and then cervical spine. Typically, two contiguous vertebrae and the interposed disk are affected. In a minority of patients, motor and sensory deficits can be seen as well. These deficits may be a result of abscess formation leading to cord compression, cauda equina syndrome, or nerve root compression or compression of the femoral nerve due to psoas abscess. Of note, psoas abscesses are common in patients with tuberculous vertebral osteomyelitis.
WBC counts are elevated in less than 50% of the patients. Normochromic anemia has been reported in three-quarters of the patients. ESR elevation is seen in more than 90% of the cases. CRP can be elevated as well. The levels of CRP may be higher in patients with pyogenic infection, rather than those with Brucella or tuberculous spinal. CRP is useful to monitor the response to therapy, as it is more closely related. CRP appears to decrease more rapidly after initiation of ultimately successful treatment for acute vertebral osteomyelitis compared with the rate of decline for ESR.
When a diagnosis of acute vertebral osteomyelitis is entertained, blood cultures should be obtained before antibiotics are initiated. At least two sets of blood cultures should be done. If blood cultures are negative and radiographic appearance is consistent with osteomyelitis, then CT-guided biopsy and aspiration, which has a sensitivity of 38% to 60%, is the next diagnostic step. Bone and disk space contents should be sent for Gram stain, aerobic and anaerobic bacterial cultures, fungal cultures, and histopathology. A second image-guided biopsy increases the diagnostic yield and can be performed if the first biopsy is negative. Alternatively, depending on the clinical scenario, empiric antibiotic therapy may be initiated in the case of a negative biopsy. Among patients with negative CT-guided biopsy or in those not responding to empiric antibiotics, an open surgical biopsy may be pursued in coordination with a spine surgeon.
Broad-range PCR of the aspirated contents is considered in scenarios when the blood cultures and disk biopsy cultures are negative.
Imaging is important not only in localizing the site of infection but also to identify other alternative diagnoses such as metastasis to the bone and osteoporotic fractures. Pyogenic complications such as epidural and psoas abscess can be visualized as well. It is reasonable to start with a plain film; however, MRI is the test of choice. It holds greater than 90% accuracy in diagnosing vertebral osteomyelitis. Normally, on the T2-weighted imaging sequences, high signal intensity is seen. When MRI cannot be done or is inconclusive, CT scan or Ga-67 citrate scanning are the alternative modalities. Positron emission tomography (PET) is a highly accurate modality that can be used in cases of patients with multifocal infection and those with spinal implants, but is limited by cost and availability.
The goals of treatment include infection eradication, to provide relief from back pain, and to prevent complications. In general, an initial 6-week course of parenteral or highly bioavailable antibiotic therapy is the standard of care. In a recently published randomized controlled trial, a 6-week course of therapy was not inferior to a 12-week course, with a cure rate above 90% in both groups. IV therapy is generally extended if there are undrained paravertebral abscesses or in patients with spinal hardware. Surgery is generally not needed, except in patients with large abscesses, patients with spinal implants, and those with spinal instability and/or progressive neurologic deficits.
Response to antimicrobial therapy should be monitored with periodic CRP values. Among patients with improvement in pain and inflammatory markers, a follow-up MRI is not recommended, as it may lead to a false impression of disease progression. However, among patients who have worsening pain, new neurologic deficits, and/or persistently elevated inflammatory markers, MRI is the appropriate radiographic study. Given the delay in response to therapy of the bony changes on MRI, focus should be on the soft tissue component of the infection.
In cases of hardware associated vertebral osteomyelitis, surgical debridement is almost always required. Infections occurring within a month of surgery are treated with debridement, retention, and a 6-week course of parenteral antibiotic therapy followed by oral suppressive therapy until the spine fuses. This may take up to 2 years. For late postsurgical hardware–associated vertebral osteomyelitis, explantation of hardware and a 6-week course of antibiotics are recommended ( Table 13.2 ).