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osteomyelitis and septic arthritis Flashcards

0
Q

What is osteomyelitis? what is it’s incidence?

A

bacterial infection of the bone, progressive inflammation and destruction of the bone.
Incidence: 2 in 10,000 ppl

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1
Q

what is septic arthritis?

A

bacterial infection of the joint

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2
Q

what is the most common bacterial in all forms of osteomyelitis?

A

staphlococcus aureus

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3
Q

how do the bacteria get into the bone?

A

hematogenous (bloodborne), contiguous spread (from nearby locatoin), trauma

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4
Q

what is acute myelitis? chronic?

A

days to weeks.

weeks to years.

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5
Q

what’s the difference between septic arthritis and reactive arthritis?

A

septic arthritis has actual pathogens in the joint space itself, while reactive arthritis is just a response to pathogens in the body (not necessarily joint space).

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6
Q

whats the most common cause of acute septic arthritis?

A

staphlococcus aureus

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7
Q

what’s another bacteria (besides s. aureus) seen in: neonates, children, very young or old, diabetics?

A

neonates (streptococci)
children (salmonella, also diabetics)
very young/old (mycoplasma hominis)

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8
Q

what is the disease for sporothrix schenckii commonly called?

A

rose gardener’s disease

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9
Q

what/why are virulence factors required for joint infections?

A 
adhesins (to attach to collagen or bone)
inflammatory stimulants (LPS or teichoic acid)
NZ that cause tissue destruction (collegenase, hyaluronase, etc. so they can use it for themselves)
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10
Q

when is septic arthritis most commonly seen?

A
  • advanced age (45% over 65 yo)

- damaged joints (RA, SLE, malignancy, diabetes)

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11
Q

what’s the predominant cause in younger adults?

A

nisseria gonorrhea

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12
Q

how many cases of septic arthritis per yr in US? Does it affect males or females more frequently?

A

20k, 7.8/100,000 (2.8/100,000) disseminated gonococcal arthritis. affects 56% males. 1/3 of patients will have significant joint damage even w/ treatment.

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13
Q

does morbidity rate for septic arthritis depend on causative agent?

A

yes, low morbidity for gonococcal arthritis but high morbidity for S. aureus.

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14
Q

what joints does septic arthritis affect most?

A

adults: knee > hip > shoulder > ankle > wrist > elbow > IP joints, sternoclavicular joints, sacroiliac joints.
Kids: hip > knee > other joints

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15
Q

How does septic arthritis break down the joints?

A

can be through the bacterial cells, can also be through our immune response to it.

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16
Q

what are some symptoms of septic arthritis?

A

swelling, redness

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17
Q

step by step septic arthritis

A

bacteria invade joint, use virulence factors and adhere to cartilage, multiply and divide, produce proteases that cause damage, signal immune system. Immune system then comes in to try to get rid of the bacteria (leads to big inflammatory response), which can lead to more damage. If it doesn’t clear the joint for a long time, can be chronic and will get prolonged destruction of joint.

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18
Q

where does a person usually get the bacteria?

A

hematogenous spread of bacteria by either direct inoculation or bacteremia (bacteria in blood), such as through UTIs, URTIs (upper respiratory tract infections), IV drug abuse, IV catheters, endocarditis, soft tissue infections. (previously damaged joints are most susceptible)

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19
Q

what is a major debilitating result of septic arthritis?

A

damage of joint cartilage

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20
Q

what does growth of bacteria in the joint and acute inflammation result in? (what immunologic response happens?)

A

PMNs infiltrate, which release inflammatory mediators and cytokines, which can damage cartilage. (bacterial proteases also damage cartilage)

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21
Q

In septic arthritis, Does N. gonorrhoeae induce a lot of inflammation or a small amount?

A

mild inflammation, probably bc they don’t have a full LPS, they just have a LOS (oligiosaccharide). This leads to less joint destruction than in S. aureus.

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22
Q

Which bacteria in septic arthritis causes recruitment of large numbers of PMNs (and therefore significant and fast joint damage)?

A

Staphlococcus aureus

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23
Q

what are some clinical manifestations of septic arthritis?

A

pain (75%), fever (40-60%), and impaired ROM. old people usually have less fever. non-gonococcal usu have pain and swelling in a single joint (80% of cases), polyarticular arthritis in 15-20% of cases, often w/ reactive and rheumatoid arthritis (often S. aureus if bacterial)
Knee > hip > shoulder > wrist > ankle > elbow

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24
Q

which type of people usually get gonococcal infection?

A

young adult, sexually active.

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25
Q

what percentage of ppl who get N. gonorrhoeae develop disseminated disease (bacteria in blood)?

A

1-3%

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27
Q

what are two ways gonorrheal infections can present in joints?

A

polyarthritis 60%(pain, fever, inflammation of tendons in wrists/fingers/ankles/toes, <12 skin lesions, joint cultures positive, blood/mucosal cultures negative), monoarticular arthritis (usually treat both the same way, but this has fewer associated symptoms) can get skin lesions in other parts of the body.

27
Q

how do you treat non-gonococcal septic arthritis?

A 
usually staph aureus, so completely drain and wash joint by arthroscopy (knee) or surgery (hip). Must not allow activated PMNs to remain in joint.  
Then parenteral (not through mouth or anus) administration of appropriate antibiotic for 3-4 wks.
even w/ correct treatment, 1/3 of patients will have significant joint damage, esp old ppl and ppl w/ preexisting joint conditions
28
Q

how do you diagnose septic arthritis?

A

collect a synovial fluid sample, send it to micro lab (will put it on chocolate agar plate [Thayer-Martin plate], followed by Gram stain where 70-80% will see Gram+. N gonorrhoeae is small grayish to colorless and mucoid, N. meningitidis is large blue-gray and mucoid)

29
Q

what is the treatment for gonococcal septic arthritis?

A

complete drainage and washing of by arthroscopy or by surgery. SAME AS NONGONOCOCCAL, EXCEPT TREATMENT IS PARENTERAL CEFTRIAXONE 24-48 HRS, THEN SWITCH TO ORAL THERAPY AFTER CLINICAL IMPROVEMENT (7-10 DAYS)

30
Q

how many cases of N. gonorrhoeae are there per year in the US?
G+ or G-?

A

1-3 million cases per yr, 1-3% develop arthritis secondary to bacteremia.
gram negative diplococci, often intracellular in PMNs
highly branched LPS (LOS)
resistant to complement
iron acquisition ability
IgA1 proteases cleave heavy chain of IgA

31
Q

what does mycobacterious tuberculosis cause (in septic arthritis)?

A

more CHRONIC monoarticular arthritis
bacteria seeded in joint via the blood
infection can involve tendon sheaths
may not have pulmonary symptoms
see with acid-fast test (aerobic acid-fast bacillus)
no Gram classification but may stain Gram positive
grows really slow in both life and in lab (test is Lowenstein-Jensen)
cell wall is peptidoglycan and high lipids
can grow intracellularly in macrophages

33
Q

tell about sporothrix schenckii in septic arthritis

A

Fungi, slow growing (so chronic monoarticular arthritis)
most common fungi of fungal arthritis
most common in knee and wrist (rose gardener’s disease).
dimorphic (cigar-shaped budding yeast in tissue specimen at body temp, hyphae w/ conidia at top of conidiophores at room temp)

34
Q

does hematogenous osteomyelitis occur most frequently in children or adults?

A

children, at the metaphysis

35
Q

what is hematogenous osteomyelitis?

A

bacteremic spread w/ seeding of bacteria in bone

36
Q

what is osteomyelitis secondary to contiguous spread?

A

follows trauma, perforation or an orthopedic procedure. Infection starts adjacent to the bone and spreads to the bone (tends to be mixed infection)

37
Q

what is diabetic foot infection?

A

osteomyelitis (specific type, secondary to contiguous spread), contiguous spread to the bone associated w/ poor vascular supply

38
Q

What is the most common pathogen for osteomyelitis for hematogenous, contiguous spread, and diabetic foot?

A

all are STAPHLOCOCCUS AUREUS.

39
Q

What is the age range for hematogenous osteomyelitis that often has streptococcus pyogenes as well?

A

1-16 years old

40
Q

What are common causative agents of osteomyelitis in infancy?

A

S. aureus, group B strep, E. coli

41
Q

What are common causative agents of osteomyelitis in childhood?

A

s. aureus, s. pyogenes, haemophilus influenzae

42
Q

What are common causative agents of osteomyelitis in adults?

A

s. aureus

43
Q

What are common causative agents of osteomyelitis in sickle cell disease?

A

salmonella, s. aureus

44
Q

What are common causative agents of osteomyelitis in trauma to the jaw?

A

actinomyces israelii (antibiotic resistant)

45
Q

What are common causative agents of osteomyelitis in immunosuppression?

A

opportunistic fungi, Nocardia sp., Pseudomonas aeruginosa

46
Q

What are common causative agents of osteomyelitis in endemic areas?

A

Coccidioides immitis, Histoplasma capsulatum

47
Q

What are common causative agents of osteomyelitis in animal exposure?

A

Brucella sp. (cats)

48
Q

What are the most common sites for hematogenous osteomyelitis?

A

spine, hip, femur, tibia, foot

49
Q

Major facts of hematogenous osteomyelitis

A

blood borne (from bacteremia), most common in prepubertal children (usually single infection site, long bones such as tibia/femur/humerus, more acute infections than adults, 1 per 5k kids, 1 per 1k neonates, in adults it’s most common in vertebrae.

50
Q

When is hematogenous osteomyelitis most prevalent?

A

diabetics (35%), after foot puncture (16%), sickle cell (0.36%)

51
Q

What is the pathogenesis of hematogenous osteomyelitis?

A

goes to actively growing metaphysis in children, which lacks many phagocytic cells, sludging off of RBCs allows formation of microclots which shield bacteria from neutrophils. bacteria then lodge in small end vessels near epiphyses. in the vertebrae, small arteriolar vessels trap the bacteria (2 adjacent vertebrae usually affected)

52
Q

symptoms of hematogenous osteomyelitis

A
  • long bone acute infections: fever, chills, malaise, pain, localized swelling and redness at site of infection in bone
  • vertebral infections: localized back pain and tenderness, maybe fever
  • chronic osteomyelitis: transient local pain, no fever usually.
  • all: Erythrocyte sedimentation rate is elevated but higher in acute than chronic. C-reactive protein levels elevated.
53
Q

diagnosis of hematogenous osteomyelitis

A

WBC counts usually normal. Use radiological procedures (xrays, CT scans, MRI). 2-3 blood cultures, if positive begin appropriate treatment, if negative deep tissue sample from adults and gram stain and histopathology exam, if negative for kid then treat empirically so you don’t mess up their epiphyseal plate.

54
Q

treatment of hematogenous osteomyelitis

A

most important to obtain a good sample for culture and histopathology for correct diagnosis and treatment, first ID microbial agent and susceptibility, then administer antimicrobial regimen for 4-6 wks.
Acute: surgery often not required
Chronic: surgery often required.

55
Q

how does treatment of hematogenous osteomyelitis vary from long bone to vertebral infections?

A

long bone you can do empiric treatment until causative pathogen is IDed (can do surgery if lots of necrotic bone).
Vertebral- don’t do empiric treatment, ID and treat based on blood, bone and soft tissue cultures (must constantly monitor patient neurological status!!!)

56
Q

how to treat different types of hematogenous osteomyelitis based on the bacteria:

  • S. aureus
  • MRSA
  • streptococci
  • enteric Gram negatives
  • Serratia or Pseudomonas
  • Anaerobes
A
  • S. aureus- nafcillin or oxacillin
  • MRSA- vancomycin
  • streptococci- penicillin G
  • enteric Gram negatives- ciprofloxacin
  • Serratia or Pseudomonas- piperacillin (tazobactam and gentamicin
  • Anaerobes- clindamycin or metronidazole
57
Q

is osteomyelitis secondary to a contiguous infection more or less complex than hematogenous? Symptoms?

A

more complex, bacteria is introduced at time of associated trauma and inflammatory response may be mild and bone damage hard to assess.
increasing pain accompanied by mild fever and minimal drainage, imaging exams are often not diagnostic.

58
Q

Are most osteomyelitis 2ndary to contiguous infection mono or polymicrobial?

A

polymicrobial

59
Q

What’s the most frequently isolated bacteria in osteomyelitis 2ndary to contiguous infection? Other common ones?

A

Staphlococcus aureus.
Pseudomonas aeruginosa- common in chronic cases, comminuted fractures, puncture wounds to the heel.
Anaerobes common in mandible infections, pressure sores, human and animal bites.

60
Q

treatment of osteomyelitis 2ndary to contiguous infection.

A

same for osteomyelitis: ID agent, test for susceptability, 4-6 wks of treatment, surgery if necessary.

61
Q

diagnosis of osteomyelitis 2ndary to contiguous infection

A

diagnosis is similar to osteomyelitis, but radiologic exams and other imaging procedures tend to not be diagnostic (need good samples for cultures)

62
Q

what are diabetic foot infections/ osteomyelitis secondary to vascular insufficiency?

A

subclass of osteomyelitis secondary to contiguous infections, in patients w/ diabetes and vascular impairment, usually lower extremities, infection progresses slowly, patient has pain and fatigue in previously traumatized skin but can lead to either no pain or excruciating pain. cellulitis (infection of skin) tends to be minimal.

63
Q

causes and signs of diabetic foot infections/ osteomyelitis secondary to vascular insufficiency

A

one bacterial cause or polymicrobial, crepitus (crackling, grating feeling or sound of joints) indicate infection w/ anaerobes or Enterobacteriaceae, Staph aureus most common causative agent
Other causative agents: Streptococcus, Enterococcus, Gram negatives (Proteus mirabilis, P. aeruginosa), anaerobes.

64
Q

diagnosis of diabetic foot infections/ osteomyelitis secondary to vascular insufficiency

A

physical exam (assess vascular supply to limb and neruopathy),
initial diagnosis w/ sterile surgical probe (if bone reached treat for osteomyelitis, if not and radiography supports then treat for soft tissue infection and follow up w/ radiograph in 2 wks),
radiograph is essential!!!

65
Q

treatment of diabetic foot infections/ osteomyelitis secondary to vascular insufficiency

A

prognosis poor bc bad vascular supply, debridement and 4-6 wks of parenteral antibiotic treatment, may require revascularization of tissue, if none of above are successful may require amputation.

66
Q

Summary of osteomyelitis:

  1. hematogenous
  2. contiguous spread
  3. Diabetic foot
A
  1. Infant (S. aureus, S. agalactiae, E. coli), children (S. aureus, S. PYOGENES, H. Influenzae), adults (S. aureus and coagulase neg staph, also gram negatives)
  2. S. Aureus, S. pyogenes, enterococcus, coagulase neg staph, gram negs, anaerobes
  3. S. aureus, strep, enterococcus, gram negs, anaerobes.
67
Q

Septic arthritis summary:

A

S. aureus (most common), N. gonnorrhoeae (young adults), gram neg bacilli (old ppl), salmonella (kids), STREPTOCOCCI (neonates), mycoplasma hominis (very young and very old), anaerobes (abdominal infections/ trauma), M. tuberculosis (chronic), borrelia borgdorferi (Lyme disease), Sporothrix schenckii (fungal; chronic)…. Almost anything

Musculoskeletal (10 decks)

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