SM_242a: Bone and Joint Infections

Question 1

Describe the pathogenesis of septic arthritis

Answer 1

Septic arthritis

• Hematogenous: vascular synovial membrane lacks a limiting basement membrane -> susceptible to deposition of bacteria during bacteremia
• Direct innoculation: surgery, trauma, or contiguous spread from adjacent infected soft tissue or bone
• Risk factors: abnormal joint, previous intraarticular steroid injection, immunosuppression, diabetes mellitus, malignancy, chronic renal failure, and IV drug abuse

Question 2

Septic arthritis can occur via _____ or _____

Answer 2

Septic arthritis can occur via hematogenous spread or direct inoculation

Question 3

Septic arthritis can spread ______ because the vascular synovial membrane lacks a limiting basement membrane, making it susceptible to deposition of bacteria during bacteremia

Answer 3

Septic arthritis can spread hematogenously because the vascular synovial membrane lacks a limiting basement membrane, making it susceptible to deposition of bacteria during bacteremia

Question 4

Pathogenesis of septic arthritis depends on _____ and _____ factors

Answer 4

Pathogenesis of septic arthritis depends on bacterial factors and host inflammatory factor

Question 5

Describe the role of bacterial factors in septic arthritis pathogenesis

Answer 5

Bacterial factors in septic arthritis pathogenesis

• Joint disease or injury facilitates bacterial adherence
• Staph aureus adhesins permit adherence to cartilage (MSCRAMMs)
• Endotoxins promote cartilage breakdown

Question 6

Describe the role of host inflammatory response in septic arthritis pathogenesis

Answer 6

Host inflammatory response in septic arthritis pathogenesis

• Host-derived extracellular proteins promote bacterial attachment
• Leukocyte-derived proteases and inflammatory cytokines cause cartilage and subchondral bone destruction
• Joint inflammation increases intra-articular pressure, reducing capillary blood flow resulting in cartilage and synovial ischemia and necrosis

Question 7

Most common etiology of septic arthritis is _____

Answer 7

Most common etiology of septic arthritis is Staphylococcus aureus

(Pseudomonas aeruginosa common in IV drug users and has predilection to involve fibrocartilaginous joints such as public symphysis and sternoclavicular and sacroiliac joints)

Question 8

Describe clinical manifestations of septic arthritis

Answer 8

Clinical manifestations of septic arthritis

• Pain and loss of function
• Swelling, redness, and increased warmth
• Fever and malaise
• Single joint (monoarticular) in 80% of cases: knee most common in adults, hip infections in kids
• Physical exam findings: infected peripheral joints (focal joint tenderness, inflammation, effusion, limited ROM), infected axial joints (focal tenderness over affected area, distant source of infection in half of patients

Question 9

Arthrocentesis of septic arthritis reveals ______ WBCs with ______ neutrophils

Answer 9

Arthrocentesis of septic arthritis reveals > 50,000 WBCs with >90% neutrophils

Question 10

Describe the differential diagnosis of fever and polyarthritis

Answer 10

Fever and polyarthritis differential diagnosis

• Infectious arthritis
• Crystal-induced arthritis: gout, pseudogout
• Post-infectious/reactive arthritis: enteric/urogenital infection (Reiter’s syndrome), rheumatic fever, inflammatory bowel disease
• Rheumatoid arthritis and Still’s disease
• Systemic rheumatic illness: systemic lupus erythematosus, vasculitis

Question 11

Empiric antibiotic therapy in septic arthritis is directed against ____ and ____

Answer 11

Empiric antibiotic therapy in septic arthritis is directed against Staphylococcus aureus and Neisseria gonorrhoeae

Question 12

Describe gonococcal arthritis

Answer 12

Gonococcal arthritis (disseminated gonococcal infection)

• Presentation: tenosynovitis, dermatitis, and polyarthralgia OR purulent monoarticular arthritis
• Epigemiology: more common in women
• Pathogenesis: occult bacteremia secondary to mucosal infection of the urethra, cervix, rectum, or oropharynx, asymptomatical mucosal infection more likely to result in disseminated gonococcal infection than symptomatic infection
• Neisseriae gonorrhoeae

Question 13

Describe Lyme Borreliosis

Answer 13

Lyme Borreliosis

• Caused by Borrelia burgdorferi
• Transmitted by Ixodes tick
• Early infection: erythema migrans (expanding annular erythematous skin lesion), disseminated infection (fever, chills, secondary annular skin lesions, meningitis, cranial neuritis, carditis, and migratory arthritis)
• Late infection: arthritis, chronic encephalopath
• 7th nerve palsy

Question 14

Describe viral arthritis caused by Parvovirus B19

Answer 14

Viral arthritis caused by Parvovirus B19

• More common in women
• Acute symmetrical polyarthritis of PIP and MCP joints with morning stiffness
• Usually results in 2 weeks (although persistent polyarticular arthritis lasting several months occurs in some female patients)

Question 15

Prosthetic joint infection is complicated by formation of _____ on the surface of prosthetic material, which _____ and _____

Answer 15

Prosthetic joint infection is complicated by formation of biofilms on the surface of prosthetic material, which slows immune response and limits antibiotic penetration

(likely Staphylococcus epidermidis)

Question 16

_____ is pathognomonic for infection

Answer 16

Sinus tract is pathognomonic for infection

Question 17

Describe treatment of prosthetic joint infection

Answer 17

Treatment of prosthetic joint infection

• Debridement with retention of prosthesis and antibiotic therapy
• One or two stage exchange and antibiotic therapy
• Long-term antibiotic therapy suppression (paliative approach)
• Implant removal without replacement and antibiotic therapy
• Amputation needed in some cases of uncontrolled infection

Question 18

_____ may be required if a prosthetic joint infection is uncontrolled

Answer 18

Amputation may be required if a prosthetic joint infection is uncontrolled

Question 19

Describe antibiotic therapy for prosthetic joint infection

Answer 19

Antibiotic therapy for prosthetic joint infection: Staphylococcal

1. Pathogen-specific IV antibiotic therapy + rifampin x2-6 weeks
2. PO rifampin + companion oral drug (ciprofloxacin or levofloxacin) x3 months (THA infection) or x6 months (TKA infection)
3. Consider indefinite chronic oral antimicrobial suppression with prosthesis debridement and retention

Question 20

Describe pathogenesis of osteomyelitis

Answer 20

Pathogenesis of osteomyelitis

• Hematogenous osteomyelitis: long bones/vertebrae/sternoclavicular joint, usually monobacterial
• Contiguous infection: sacrum/pelvis/foot adjacent to neuropathic ulcers, usually polymicrobial
• Escape host defeneses: adherence to damaged bone, persistence within osteoblasts, microorganisms coat themselves and underlying bone surfaces with biofilm

Question 21

Osteomyelitis pathogenesis is either ____ or ____

Answer 21

Osteomyelitis pathogenesis is either hematogenous or contiguous

Question 22

Hematogenous osteomyelitis is usually ____ and occurs in ____, ____, and ____

Answer 22

Hematogenous osteomyelitis is usually monobacterial and occurs in long bones, vertebrae, and sternoclavicular joint

Question 23

Contiguous osteomyelitis is usually ____ and occurs in the ____, ____, and ____ adjacent to ____

Answer 23

Contiguous osteomyelitis is usually polymicrobial and occurs in the sacrum, pelvis, and foot adjacent to neuropathic ulcers

Question 24

Osteomyelitis escapes host defenses via _____, _____, and _____

Answer 24

Osteomyelitis escapes host defenses via adherence to damaged bone, persistence within osteoblasts, and microorganisms coating themselves and underlying bone surfaces with biofilm

Question 25

Pathogenesis of osteomyelitis caused by Staphylococcus aureus involves _____ and _____

Answer 25

Pathogenesis of osteomyelitis caused by Staphylococcus aureus involves binding to fibronectin/collagen/sialylglycoprotein on bone surface and surviving in a dormant and phenotypically altered state within osteoblasts

(binding via MSCRAMMs, dormant state explains long incubation period and high relapse rate of Staph aureus osteomyelitis treated with a short course of antibiotics)

Question 26

Biofilms ____, ____, and ____

Answer 26

Biofilms facilitate gene transfer of virulence factors and antibiotic resistance, evade host immune response via rapid changes in antigen expression, and antibiotic resistance by slowing diffusion and causing antibiotic malfunction

(biofilm: organized group of microorganisms in extracellular polymeric matrix)

Question 27

Most common microorganism cause of osteomyelitis is _____

Answer 27

Most common microorganism cause of osteomyelitis is Staphylococcus aureus

Question 28

Describe clinical manifestations of osteomyelitis

Answer 28

Clinical manifestations of osteomyelitis

• Subacute-to-chronic presentation
• Nonspecific pain around the involved site
• Fever, chills, and local swelling and erythema in the proximity of the involved bone infrequently
• Draining sinus tract over the involved bone occassionally

Question 29

Absent sepsis, in osteomyelitis ____ antibiotic therapy until adequate specimens are sent for culture

Answer 29

Absent sepsis, in osteomyelitis delay antibiotic therapy until adequate specimens are sent for culture

Question 30

Vertebral ostoemyelitis involves _____ spread

Answer 30

Vertebral ostoemyelitis involves hematogenous spread

(organisms reach the well-perfused vertebral body via spinal arteries and spread from the end plate into the disk space and then to the adjacent vertebral body)

Question 31

Pott’s disease is _____ due to _____

Answer 31

Pott’s disease is vertebral osteomyelitis due to Mycobacterium tuberculosis

Question 32

Pathogenesis of diabetic foot infection involves _____, _____, and _____

Answer 32

Pathogenesis of diabetic foot infection involves neuropathy, vascular insufficiency, and hyperglycemia

(neuropathic skin ulceration, contiguous osteomyelitis)

Question 33

Diabetic foot infection is treated with _____, _____, and _____

Answer 33

Diabetic foot infection is treated with revascularization when indicated, surgical debridement of infected bone and soft tissue, and broad-spectrum antibiotic therapy (ideally following intraoperative deep cultures) aimed at aerobic and anaerobic bacteria

Question 34

Probe to bone in diabetic function likely indicates _____

Answer 34

Probe to bone in diabetic function likely indicates osteomyelitis

Question 35

Describe treatment of osteomyelitis

Answer 35

Treatment of osteomyelitis

• Goals of therapy: eradicate infection, restore function
• Combination medical and surgical therapy: prolonged antimicrobial therapy for 4-6 weeks (no evidence that longer duration improves outcomes), 20% relapse rate despite aggressive therapy

Question 36

_____ are better than _____ antibiotics for penetration into bone, with _____ having the greatest penetration

Answer 36

Oral are better than IV antibiotics for penetration into bone, with rifampin having the greatest penetration

Question 37

High relapse rate with osteomyelitis is secondary to _____

Answer 37

High relapse rate with osteomyelitis is secondary to biofilm formation on devascularized bone

Question 38

Drainage of infected synovial fluid in cases of septic arthritis is necessary because _____

Answer 38

Drainage of infected synovial fluid in cases of septic arthritis is necessary because inflammatory synovial fluid destroys cartilage

Question 39

Summarize bone and joint infections

Answer 39

• Septic arthritis: usually hematogenous, arthrocentesis shows > 50,000 WBCs predominantly neutrophils, typically monomicrobial (Staphylococcus aureus and Neisseria gonorrhoeae), and drainage of inflammatory fluid
• Osteomyelitis: hematogenous in long bones/vertebrae due to Staphylococcus aureus, contiguous in foot/sacrum and polymicrobial
• MRI: sensitive and specific
• Debridegement of dead bone and prolonged antibiotic therapy