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MSK/Derm > Bone and Joint Infections > Flashcards

Bone and Joint Infections Flashcards

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1
Q

What are the long term impacts on joints of bacterial vs. viral vs. mycobacteria/non-Candida fungi arthritis?

A

bacterial - rapid joint destruction with irreversible loss of function

viral - generally does not lead to long-term joint damage

mycobacteria/non-Candida fungi - slowly progressive monoarticular arthritis

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2
Q

What is the pathogenesis of septic arthritis?

A

hematogenous - vascular synovial membrane lacks a limiting basement membrane and is particularly susceptible to the deposition of bacteria during bacteremia

direct innoculation from surgery, trauma, or contiguous spread

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3
Q

What are the risk factors for getting septic arthritis?

A

abnormal joint

immunosuppression

diabetes mellitus

malignancy

chronic renal failure

intravenous drug abuse

previous intraarticular steroid injections

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4
Q

What are the bacterial factors that allow certain species to cause spetic arthritis?

A

joint disease or injury facilitates bacterial adherence

Staphylococcus aureus adhesins permit adherence to cartilage - MSCRAMMs (microbial surface components recognizing adhesive matrix molecules)

endotoxins promote cartilage breakdown

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5
Q

What are the host inflammatory responses that lead to septic arthritis?

A

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

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6
Q

What common bacteria causes septic arthritis?

A

gram positive cocci - S. aureus, S. pyogenes, S. agalactiae

gram negative bacilli - E. coli, P. aeruginosa (fibrocartilaginous joints), K. kingae

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7
Q

What are some unusual bacterial pathogens that lead to septic arthritis?

A
  • Pasteurella multocida*, capnocytophaga spp. from dog or cat bites
  • Eikenella corrodens* from a human bite
  • Borrelia burgdorferi* (Lyme disease)
  • Tropheryma whipplei* (Whipple’s disease)
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8
Q

What are the clinical manifestations of septic arthritis?

A

pain and loss of function

swelling, redness, and increased warmth

fever and malaise

single join (monoarticular) in 80% of cases - knee most common (50%), shoulder, wrist, ankle, hips (in children)

infected peripheral joints

infected axial joints

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9
Q

What are physical examination findings in septic arthritis?

A

infected peripheral joints including focal joint tenderness, inflammation and effusion

active and passive range of motion limited and results in discomfor

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10
Q

What are the lab findings in septic arthritis?

A

elevated ESR and CRP

arthrocentesis reveals >50,000 WBC with >90% neutrophils

can see >100,000 with RA flare, leukemia, gout, reaction to intraarticular injection

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11
Q

What is seen in x-rays in septic arthritis?

A

early infection - periarticular soft tissue swelling and normal bone

advanced infection - joint space loss, periosteal reaction, and destruction of subchondral bone

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12
Q

What is the role of ultrasound in septic arthritis?

A

extremely sensitive to confirm the presence of effusion and used to guide needle aspiration of certain joints

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13
Q

What is the role of CT and MRI in septic arthritis?

A

sensitive for early septic arthrits

in CT, can see erosive bone changes, joint effusions, and periarticular soft tissue extension of infection

MRI is simply more specific than CT

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14
Q

What is the differential diagnosis of fever and polyarthritis?

A

infectiuos arthritis

crystal-induced arthritis - gout and pseudogout

postinfectious or reactive arthritis - Reiter’s Syndrome, rheumatic fever, and inflammatory bowel disease

rheumatoid arthritis and Still’s disease

systemic rheumatic illness - SLE and vasculitis

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15
Q

What is the treatment for septic arthrits?

A

joint drainage - repeated arthrocentesis and arthroscopic lavage

antibiotic therapy empiric for S. aureus and N. gonorrhoeae

specific therapy based on blood or synovial fluid culture results

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16
Q

What is the clinical presentation of gonococcal arthritis?

A

tenosynovitis, dermatitis, and polyarthralgia

or

purolent monoarticular arthritis

17
Q

What is the epidemiology of Gonococcal arthritis?

A

4 times more common in women than men

complicates 0.5%-3% of cases with mucosal gonococcal infection

18
Q

What is the pathogenesis of gonococcal arthritis?

A

occult bacteremia secondary to mucosal infection of urethra, cervix, rectum, or oropharynx

asymptomatic mucosal infection more likely to result in disseminated gonococcal infection (DGI) than symptomatic infection

Neisseria gonorrhoeae - surface glycoproteins undergo phase and antigenic variation

persistent infection increases opportunity for invasive, serum-resistant straints to emerge

19
Q

What are the clinical features of Gonococcal arthritis?

A

triad of dermatitis, tenosynovitis, and migratory polyarthralgia or polyarthritis - tenosynovitis involves fingers, hands, and wrists

septic arthritis with a purulent joint effusion - clinically indistinguishable from bacterial arthritis caused by other organisms

low yield from blood and synovial cultures - mucosal infection usually present

20
Q

What are the skin lesions in Gonococcal arthritis?

A

macules

papules

pustules on an erythematous base

may develop central necrosis

few in number, painless

21
Q

What is lyme borreliosis?

A

most common vector-borne infection in the US

caused by Borrelia burgdorferi

transmitted by the Ixodes tick - prevalent in northeastern and upper Midwest US

early infection - erythema migrans (EM)

disseminated infection with fever, chills, secondary annular skin lesions, meningitis, cranial neuritis, carditis and migratory arthritis

late infection - arthritis and chronic encephalopathy

22
Q

What causes viral arthritis?

A

human parovirus B19

aka “fifth disease” or “erythema infectiosum”

arthritis or arthralgias more common in women than men (60% vs 30%)

acute symmetrical polyarthritis of PIP and MCP joints with morning stiffness

usually resolves within 2 weeks

23
Q

What are classical childhood skin rashes?

A

measles

scarlet fever

rubella

Duke’s disease

Fifth disease (erythema infectiosum)

Roseola (exanthem subitum)

24
Q

What causes chronic infectious arthritis?

A

in healthy hosts, Blastomyces dermatitidis and Coccidioides spp

in immunocompromised hosts, Candida spp., Cryptococcus, Aspergillus

Tuberculosis - 10% of extrapulmonary TB involves the bone and joints (1% to 3% of all TB cases)

25
Q

How does prostetic joint infections occur?

A

often results from intraoperative contamination of the prosthesis by skin microorganisms

biofilm formation on the surface of prosthetic material - retards immune response, limits antibiotic penetration

26
Q

What is the treatment for prosthetic joint infection?

A

debridement with retention of preosthesis and antibiotic therapy

one- or two-stage exchange and antibiotic therapy

long-term antimicrobial suppression (palliative appraoch)

implant removal without replacement and antibiotic therapy - amputation needed in some cases of uncontrolled infection

27
Q

What is the pathogeneis of osteomyelitis?

A

hematogenous osteomyelitis - long bones, vertebrae, sternoclavicular joint, usually monobacterial

contiguous infection - sacrum, pelvis, foot - adjacent to neuropathic ulcers, usually polymicrobial

escapes host defenses - adherence to damaged bone, persistence with osteoblasts, microorganism caots themselves and underlying bone surfaces with biofilm

form sequestra - pus spreads into vascular channels, raise intraosseous pressure an dimpairs blood flow-> ischemic necrosis of bone results in separation of large devascularized fragments (sequestra)

28
Q

How does S. aureus cause osteomyelitis?

A

bind to fibronectin, collagen or sialoglycoprotein present on bone surface (MSCRAMMs)

survive in a dormant and phenotypically altered state within osteoblasts (renders S. aureus more resistant to the action of antibiotics)

this may explain long incubation period and high relapse rate

29
Q

What are the possible etiologies for osteomyelitis?

A

S. aureus - most frequent along with Peptostreptococcus spp.

coagulase-negative staphylococci - foreign body

enterobacteriae - common in nocosomial infections

P. aeruginosa - nosocomial, nail puncture wounds in foot

streptococci or anaerobic bacteria - bites, diabetic food lesions, decubitus ulcers

Pasteurella multocida or Eikenella corrodens - animal and human bites

Aspergillus, Mycobacterium avium complex, or Candida albicans - immunocompromised

Mycobacterium tubeculosis, Brucella, Coxiella burnetii, endemic fungi - endmic populations

30
Q

What are the clinical manifestations of osteomyelitis?

A

subacute-to-chronic presentation

nonspecific pain around the involved site

fever, chills, and local swelling and erythema in the proximity of the involved bone - infrequent

draining sinus tract over the involved bone - occasional

31
Q

What are the common lab tests for osteomyelitis?

A

peripheral leucocyte countes, ESR, and C-reactive protein

32
Q

What are the radiologic tests for osteomyelitis?

A

conventional x-rays - can see abnormalities 10-14 days after onset

nuclear bone scans - sensitive but nonspecific

CT and MIR - standard of care

33
Q

What is the treatment for osteomyelitis?

A

prolonged antimicrobial therapy (6-12 weeks)

20% relapse rate despite aggressive therapy

surgical therapy - debridement of infected tissue

34
Q

What are the causes of vertebral osteomyelitis?

A

infection involving:

  • intervertebral disk
  • adjacent vertebrae
  • with or without associated epidural os psoas abscesses

hematogenous - 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

35
Q

What is the clinical presentation of vertebral osteomyelitis?

A

localized insiduous pain and tenderness in the spine

fever < 50%

motor and sensory deficits (spinal cord or nerve root compression) 15%

36
Q

What is Pott’s Disease?

A

tuberculous spondylitis

vertebral osteomyelitis due to Mycobacterium tuberculosis

systemic symptoms often absent

back pain or stiffness is commonly the only symptom

delayed diagnosis is common

abnormal chest x-ray < 50%

37
Q

What is the cause of diabetic foot?

A

osteomyelitis in patients with diabets - typically involves foot and 15% develop foot ulcers during their lifetime

pathogenesis - neuropathy, vascular insufficiency, and hyperglycemia

neuropathic skin ulceration with contiguous osteomyelitis

38
Q

What is the treatment for diabetic foot?

A

revascularization (when indicated) - for patients with poor arterial vascular supply

surgical debridement of infected bone and soft tissue

broad-spectrum antibiotic therapy (ideally following intraoperative deep cultures) aimed at aerobic and anaerobic bacteria

MSK/Derm (54 decks)

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