39
Etiology and Pathogenesis of Musculoskeletal Infections

Etiology and pathogenesis

Embed Size (px)

Citation preview

Page 1: Etiology and pathogenesis

Etiology and Pathogenesis of Musculoskeletal Infections

Page 2: Etiology and pathogenesis

Etiology

• Commonly occurs in childhood.• More common in males• Malnutrition• History of injury.

Page 3: Etiology and pathogenesis

Pathophysiology

• Adult osteomyelitis• Pediatric osteomyelitis• Septic arthritis.

Page 4: Etiology and pathogenesis

Pathophysiology of osteomyelitis

• age of the host• duration of infection– < 6 weeks- acute– > 6 weeks- chronic

• etiology of infection• type of host response to the infection

Page 5: Etiology and pathogenesis

Routes

• Exogenous- direct inoculation of the bone from either trauma, surgery, or a contiguous focus of infection.

• Hematogenous- via the vascular tree into either osseous or synovial tissue, producing a localized focus of infection.

• Local tissue compromise or systemic tissue (i.e., diabetes) compromise associated with an increased risk.

Page 6: Etiology and pathogenesis
Page 7: Etiology and pathogenesis

Response

• Pyogenic organisms- rapidly progressive course of pain, swelling, abscess formation, and aggressive bone destruction.

• Less aggressive nonpyogenic organisms(eg AFB) invoke a more insidious granulomatous reaction.

Page 8: Etiology and pathogenesis

• Age of the host is important in that differences in bone vascular anatomy between adults and children slightly alter the mechanism of hematogenous delivery.

• Children are susceptible to different organisms depending upon their age.

Page 9: Etiology and pathogenesis

Exogenous osteomyelitis

• clearly identified anatomic site, • inoculated with pyogenic organisms,• polymicrobial, • frequently in association with foreign debris.

Page 10: Etiology and pathogenesis

• Bacteria inoculated into a compromised local environment,

• Bone and soft tissue disruption providing ample amounts of necrotic and devascularized material favorable for bacterial growth.

Page 11: Etiology and pathogenesis

• Tissue devascularization prevents host response mechanisms from reaching bacterial colonies, thereby permitting unchecked proliferation.

Page 12: Etiology and pathogenesis

Host response to injury

• Activation of inflammatory and immunologic pathways.

• Inflammatory elements serve to destroy bacteria and remove nonviable material.

• Humoral and cellular immunologic mechanisms act to recognize specific bacteria and subsequently confer immunity to prevent further bacterial dissemination.

Page 13: Etiology and pathogenesis

Inflammatory pathway

• Increases in blood flow• vascular permeability• delivery of polymorphonuclear leukocytes• Mononuclear cells arrive within 24 to 48 hours

and assist in eradication of bacteria and removal of necrotic bone.

• Pus and abcess formation.

Page 14: Etiology and pathogenesis

• Granulation tissue surrounds the infected area in an attempt to wall off the infection.

• Reactive bone formation occurs to further sequester the infection from the host.

• Within the infected region, dead bone is often prominent, and this is commonly termed the sequestrum, whereas the reactive bone is known as the involucrum

Page 15: Etiology and pathogenesis

• This area is isolated from host defense mechanisms by the avascular fibrous tissue and can permit the continued proliferation of bacteria

Page 16: Etiology and pathogenesis

Bacterial adhesions

• Acquiring of a glycoproteinaceous conditioning film when exposed to a biologic environment over the tissue- or implant-derived surfaces.

• This surface is anionic that repels the anionic covering of the bacteria initially.

Page 17: Etiology and pathogenesis

• However, attractive forces (van der Waals), in conjunction with hydrophobic molecules on the exposed substrate and the bacteria, increase the duration of bacterial juxtaposition.

• Formation of irreversible cross-links between bacteria and host surfaces

Page 18: Etiology and pathogenesis

• Proliferation occurs with formation of a polysaccharide slime layer.

• The biofilm or slime layer is composed of bacterial extracapsular exo-polysaccharides that bind to surfaces, thereby promoting cell-to-cell adhesion, microcolony formation, and layering of the microorganisms.

Page 19: Etiology and pathogenesis

• Additional species of bacteria may attach to the surface of the biofilm, resulting in syntropic interactions between differing bacteria

Page 20: Etiology and pathogenesis
Page 21: Etiology and pathogenesis
Page 22: Etiology and pathogenesis

Properties of biofilm

• Bacterial attachment in production of biofilms can lead to antibiotic resistance.

• Decreased metabolic rates and phenotypic changes in surface-adherent bacteria.

Page 23: Etiology and pathogenesis

Pediatric Osteomyelitis

• Hematogenous inoculation.• Pediatric bones more predisposed due to their

vascular anatomy.• The nutrient artery of long bones enters

through the cortical bone to divide within the medullary canal, ending in small arterioles that ascend toward the physis.

Page 24: Etiology and pathogenesis
Page 25: Etiology and pathogenesis

• Just beneath the physis, these arterioles bend away from the physis and empty into venous lakes within the medullary cavity.

• The acute bend in these arterial loops serve as points of diminished blood velocity, promoting sludging of bacteria directly under the physis.

Page 26: Etiology and pathogenesis
Page 27: Etiology and pathogenesis

• In addition, phagocytic capability and reticuloendothelial function may be depressed in these vascular loops, promoting the establishment of bacterial colonies.

• Trauma, often associated with the emergence of osteomyelitis in children, may actually promote bacterial seating and proliferation in metaphyseal sites.

Page 28: Etiology and pathogenesis
Page 29: Etiology and pathogenesis

• This pus can spread in one of three ways: through the physis, toward the diaphysis, or through the adjacent bony cortex.

• This purulent material tends to seek the path of least resistance, through the metaphyseal cortex, to form a collection of subperiosteal pus.

Page 30: Etiology and pathogenesis
Page 31: Etiology and pathogenesis

• Although this is the most common route of egress, younger children (less than 1 year) with intact transphyseal vessels may demonstrate epiphyseal spread with the development of epiphyseal abscesses.

• In older children, the development of a subperiosteal abscess results in devascularization of the bone both from thrombosis of the endosteal blood supply and from the stripping away of the overlying periosteum.

Page 32: Etiology and pathogenesis

• The periosteum, which is extremely thick and loosely adherent in children, is not easily penetrated; in the devascularization process, it is lifted off the bone, with the inner cambium layer producing a layer of new bone.

• In this case, the devascularized bone is termed the sequestrum, with the reactive periosteal bone being the involucrum

Page 33: Etiology and pathogenesis
Page 34: Etiology and pathogenesis

• A cellulitic phase precedes abscess formation, with medical management alone being successful to cure the infection.

• Once an abscess forms, surgical debridement is necessary to remove the nonviable bone, reduce the bacterial population, and provide for a vascularized tissue bed for antibiotic delivery.

Page 35: Etiology and pathogenesis

• Staphylococcus aureus (90%) • In neonates, the most common organisms

include Staphylococcus aureus, group B streptococci, and gram-negative organisms

Page 36: Etiology and pathogenesis

Pediatric septic arthritis

• Acute septic arthritis may develop from hematogenous sources or, more commonly, from extension of an adjacent foci of osteomyelitis into the joint.

• Susceptible joints are those in which the metaphysis is intra-articular, such as seen in the hip and shoulder where bacteria are afforded an avenue for dissemination.

Page 37: Etiology and pathogenesis
Page 38: Etiology and pathogenesis
Page 39: Etiology and pathogenesis