SM_242a: Bone and Joint Infections Flashcards
(39 cards)
Describe the pathogenesis of septic arthritis
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
Septic arthritis can occur via _____ or _____
Septic arthritis can occur via hematogenous spread or direct inoculation

Septic arthritis can spread ______ because the vascular synovial membrane lacks a limiting basement membrane, making it susceptible to deposition of bacteria during bacteremia
Septic arthritis can spread hematogenously because the vascular synovial membrane lacks a limiting basement membrane, making it susceptible to deposition of bacteria during bacteremia
Pathogenesis of septic arthritis depends on _____ and _____ factors
Pathogenesis of septic arthritis depends on bacterial factors and host inflammatory factor
Describe the role of bacterial factors in septic arthritis pathogenesis
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
Describe the role of host inflammatory response in septic arthritis pathogenesis
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
Most common etiology of septic arthritis is _____
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)
Describe clinical manifestations of septic arthritis
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
Arthrocentesis of septic arthritis reveals ______ WBCs with ______ neutrophils
Arthrocentesis of septic arthritis reveals > 50,000 WBCs with >90% neutrophils

Describe the differential diagnosis of fever and polyarthritis
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

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

Describe Lyme Borreliosis
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
Describe viral arthritis caused by Parvovirus B19
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)
Prosthetic joint infection is complicated by formation of _____ on the surface of prosthetic material, which _____ and _____
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)

_____ is pathognomonic for infection
Sinus tract is pathognomonic for infection

Describe treatment of prosthetic joint infection
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

_____ may be required if a prosthetic joint infection is uncontrolled
Amputation may be required if a prosthetic joint infection is uncontrolled
Describe antibiotic therapy for prosthetic joint infection
Antibiotic therapy for prosthetic joint infection: Staphylococcal
- Pathogen-specific IV antibiotic therapy + rifampin x2-6 weeks
- PO rifampin + companion oral drug (ciprofloxacin or levofloxacin) x3 months (THA infection) or x6 months (TKA infection)
- Consider indefinite chronic oral antimicrobial suppression with prosthesis debridement and retention
Describe pathogenesis of osteomyelitis
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
Osteomyelitis pathogenesis is either ____ or ____
Osteomyelitis pathogenesis is either hematogenous or contiguous
Hematogenous osteomyelitis is usually ____ and occurs in ____, ____, and ____
Hematogenous osteomyelitis is usually monobacterial and occurs in long bones, vertebrae, and sternoclavicular joint
Contiguous osteomyelitis is usually ____ and occurs in the ____, ____, and ____ adjacent to ____
Contiguous osteomyelitis is usually polymicrobial and occurs in the sacrum, pelvis, and foot adjacent to neuropathic ulcers
Osteomyelitis escapes host defenses via _____, _____, and _____
Osteomyelitis escapes host defenses via adherence to damaged bone, persistence within osteoblasts, and microorganisms coating themselves and underlying bone surfaces with biofilm






