Infectious Disease of the Bone and Joint PDF
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Uploaded by HumbleChrysanthemum
Eastern Mediterranean University
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Summary
This document provides an overview of infectious diseases affecting bones and joints, including their causes, symptoms, and treatments. It covers various types such as pyogenic osteomyelitis, infectious arthritis, and Lyme arthritis, and highlights the clinical features and mechanisms associated with each.
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Infectious disease of the bone and joint Pyogenic Osteomyelitis Most cases of acute osteomyelitis are caused by bacteria Staphylococcus aureus is the most common agent. Escherichia coli and group B streptococci in neonates, Salmonella is common in sickle cell disease. Mixed bacterial infections -- s...
Infectious disease of the bone and joint Pyogenic Osteomyelitis Most cases of acute osteomyelitis are caused by bacteria Staphylococcus aureus is the most common agent. Escherichia coli and group B streptococci in neonates, Salmonella is common in sickle cell disease. Mixed bacterial infections -- secondary to bone trauma. In as many as 50% of cases, no organism can be isolated. Three routes: (1) hematogenous dissemination (most common); (2) extension from an infection in adjacent joint or soft tissue (3) traumatic implantation after compound fractures or orthopaedic procedures. Causal bacteria proliferate=> acute inflammatory reaction=>Cell death => sequestrum (Bone necrosis; and non-viable bone) Bacteria and inflammation subperiosteal abscesses haversian systems Blood supply impairment Rupture of periosteum=> soft tissue abcess, sinus Spread into the adjoining joint => suppurative arthritis (infants, not adults) suppurative and ischemic injury necrosis After the first week of infection, chronic inflammatory cells become more numerous. Leukocyte cytokines=> osteoclastic bone resorption, fibrous tissue ingrowth, and bone formation in the periphery. Reactive woven or lamellar bone deposition forming a shell of living tissue around a sequestrum is called an involucrum Viable organisms can persist in the sequestrum for years after the original infection. Clinical Features Acute systemic illness (malaise, fever, leukocytosis, and throbbing pain). Sometimes subtle... The diagnosis is suggested by characteristic radiologic findings: a destructive lytic focus surrounded by edema and a sclerotic rim. A combination of antibiotics and surgical drainage usually is curative, but up to a quarter of cases do not resolve and persist as chronic infections. Acute flareups + complications (pathologic fracture, secondary amyloidosis, endocarditis, sepsis, development of squamous cell carcinoma and rarely osteosarcoma) Infectious Arthritis Microorganisms of any type Serious, because it can cause rapid joint destruction and permanent deformities. Suppurative Arthritis Any bacteria can be causal, but Haemophilus influenzae predominates in children younger than 2 years of age S. aureus is the main causative agent in older children and adults Sickle cell disease are prone to Salmonella infection at any age. Sudden onset of pain, redness, and swelling of the affected joint(s), with restricted range of motion. Fever, leukocytosis, and elevated erythrocyte sedimentation rate are common. Lyme Arthritis Borrelia burgdorferi, transmitted by ticks Lyme disease involves multiple organ systems Stage 1 - Multiply at the site of the tick bite and cause an expanding area of redness=>erythema chronicum migrans Stage 2 - the early disseminated stage, Spread hematogenously => secondary annular skin lesions, lymphadenopathy, migratory joint and muscle pain, cardiac arrhythmias, and meningitis, often with cranial nerve involvement. Diagnostic antibodies (IgM and IgG) against Borrelia antigens appear in the serum at this stage Stage 3 -the late disseminated stage. 2 or 3 years after the initial bite. Lyme Borrelia organisms cause a chronic arthritis, sometimes with severe damage to large joints, and an encephalitis. Lyme arthritis is the dominant feature of late disease. The arthritis may be caused by immune responses against Borrelia antigens that cross-react with proteins in the joints, but the exact mechanisms are not yet understood. The disease tends to be migratory, with remissions and relapses. Mainly large joints Histologic examination: Chronic papillary synovitis with synoviocyte hyperplasia, fibrin deposition, mononuclear cell infiltrates, and onionskin thickening of arterial walls silver stains reveal a organisms in only %25 of cases Diagnosis of Lyme arthritis => clinical picture, history, serologic studies. Chronic arthritis with pannus formation and permanent deformities develops in roughly 1 in 10 patients. Osteonecrosis (Avascular Necrosis) Ischemic necrosis with resultant bone infarction Mechanisms: Vascular compression or disruption (e.g., after a fracture) Steroid administration Thromboembolic disease (nitrogen bubbles in caisson disease) Primary vessel disease (e.g., vasculitis) Sickle cell crisis Subchondral infarcts =>pain during physical activity May collapse and lead to severe osteoarthritis. Medullary infarcts usually are silent Dead bone with empty lacunae is interspersed with areas of fat necrosis The cortex usually is not affected, because of collateral blood supply; in subchondral infarcts, the overlying articular cartilage also remains viable because the synovial fluid can provide nutritive support. Tuberculous Osteomyelitis 1% to 3% of cases of pulmonary tuberculosis. The organisms usually reach the bone through the bloodstream, Long bones and vertebrae are favored sites. Tubercle bacillus is microaerophilic=> the synovium, a high oxygen pressure area, a common site of initial infection. Spreading to the adjacent epiphysis=>granulomatous inflammation and bone destruction. Pott disease: Tuberculosis of the vertebral bodies=> deformity, posterior displacement=> neurologic deficits. Psoas muscle abscesses is fairly common.