Osteomyelitis and Implant Infections Flashcards
what is osteomyelitis?
inflammation of the bone marrow, cortex, and possibly the periosteum; can be
acute: systemic illness, pain, and soft tissue swelling without radiographic change; rapid onset of clinical signs (within days); use gram staining to guide diagnosis allowing for rapid treatment, but should perform culture and susceptibility too
chronic: systemic illness may have subsided, have a draining tract, may see cellulitis, abscess, and/or progressive or destructive osseous change on radiographs; typically require radical surgical excision and removal of implant may be required
define cloaca, involucrum, and sequestra
sequestra: fragments of necrosed bone that separate from surrounding tissue
involucrum: the bone bed the sequestrum came from
cloaca: the track the sequestra takes
what are 3 sources of bone infection?
- infectious agent gets into traumatic or surgical wound; bacteria (staphylococcus and streptococcus very common), mycotic infections, viruses, parasites, foreign bodies, implant, lumpy jaw in cattle
- hematogenous: more common in juveniles due to failure of passive immunity or concurrent infection (septicemia, septic oomphalitis); bacteremic seeding of bone from a distant source of infection
- contiguous spread from surrounding tissue and joints
common causes: gunshot wounds, HBC, and bite wounds (esp cats)
what bacteria causes over half of the osteomyelitis cases in animals?
beta lactamase producing staphylococcus species, but many other bacteria cause as well with the potential for polymicrobial infections
describe the anatomy/physiology that lead to septic arthritis (3)
- lack of basement membrane in synovium means easy translocation of an infection near the joint into the joint
- synovial villi: are like seaweed, so bacteria can get stuck in them and stay protected
- synovium releases inflammatory mediators, enzymes, and free radicals that have a positive feedback effect to exacerbate the problem into an osteoarthritic cycle
describe the general pathogenesis of osteomyelitis (7)
- extent of soft tissue damage allow an excellent blood culture media for bacteria
- alteration of blood supply due to damage both increases potential for necrosis and decreases the body’s ability to fight infection
- foreign material potentiates bacterial proliferation
- biofilm formation allows bacterial adhesion and protection from phagocytosis; microbes produce hyaluronidases, collagenases, and proteases to break down bone matrix
- subchondral or metaphyseal bone inoculation with microbes results in local infiltration of neutrophils
- initiation of demineralization is osteolysis (direct and indirect mechanisms)
- microbial and cellular debris occlude blood supply and lead to avascular necrosis in the haversian and volkmann’s canals; necrotic bone breaks off as sequestra, leading to circumferential bone loss at the involucrum, resulting in peripheral hyperemia and increased reactive bone
describe some species specific factors of osteomyelitis in dogs and cats (5)
- most common causes are trauma (HBS) and site specific infections (bite wounds)
- 88% of cultures are positive for staphylococcus spp.
- cats most commonly affected by infected soft tissue
- dogs most common affected by closed fractures
- osteomylelitis has been reported up to 11% with prostheses
describe some species specific factors of osteomyelitis in horses (4)
- relatively common (have very little skin coverage in distal limbs, common injury site
- in foals, most common bacterial agents are: enterobacteriaceae, streptococcus, and staphylococcus, respectively, plus rhodococcus for older wenalings
- polymicrobial osteomylelitis is more common in foals than in dogs and cats
- there is increased concern regarding osteomyelitis in horses due to the possibility of developing support limb laminitis in the non-osteomyelitic limb
describe some species specific factors of osteomyelitis in cattle (5)
- common agent is trueperella pyogenes
- neonates also develop osteomyelitis due to chain trauma from dystocia
- post-op not as common (we’re not putting bone plates in cattle)
- hematogenous route is 3x more likely than trauma!!!! in all ages
- if osteomyelitis in the digit, can actually amputate the digit with relative success
what are bacterial biomaterials?
non-living surfaces that serve as adherence site for bacteria
- indwelling catheters
- prostheses
- implants
what are bacterial biofilms?
highly structured communities of bacteria that enable cell to cell communication and allow bacteria to adapt to stressors such as changes in pH, osmolarity, and temperature as well as develop antibiotic tolerance (increase minimum inhibitory concentration up to 100 fold)
how do biofilms resist antimicrobials? (7)
- limited diffusion of antimicrobial through biofilm
- enzyme mediated destruction
- changes in cell wall permeability
- alterations to structure
- mutations in efflux mechanism
- bypass metabolic pathways
- hypoxic low metabolic state works against antimicrobials requiring metabolic activity
what are 3 ways bacterial increase their virulence to evade the host? what dilemma does this put us in when the source of the bacteria is an implant or prosthesis?
- bacterial adhesion molecules
- exotoxin production (hemolysin, leukotoxin)
- production of biofilm via extracellular glycocalyx
this makes life hard when the source is an implant or prosthesis; the dilemma is do you remove the implant potentially too early and risk bone healing, or do you leave the implant and risk infection/osteomyelitis?
do we have many options for antibiotics to treat biofilms? describe
no!
staphylococci is the most commonly isolated organism in clinical osteomyelitis and the only Ab we have for staph biofilm is rifampicin, which is only approved for use in humans
for gram negative biofilms, ciprofloxacin is the Ab of choice
generally for vet patients there is limited availability of effective antibiotics and fewer repots of efficacy
what are the stages of biofilm formation, and what stage do you really want to try to treat before?
- attachment
- cell to cell adhesion
- proliferation
- maturation
- dispersion to attach somewhere else and form another biofilm
really want to handle the infection before the proliferation phase, becomes much more difficult after that
