Infections of bones and joints Flashcards
What are the pathological changes seen in acute versus chronic osteomyelitis?
Acute osteomyelitis presents with inflammatory infiltration, pus formation, and bone destruction, whereas chronic osteomyelitis is characterized by necrotic bone (sequestrum), fibrosis, and the formation of sinus tracts.
What is the pathophysiology of hematogenous osteomyelitis?
Bacteria enter the bloodstream, seed in the bone’s vascular metaphysis (especially in children), evade host defenses, proliferate, and induce an inflammatory response, leading to tissue destruction and potential sequestrum formation.
Why is vertebral osteomyelitis common in adults?
The vertebral column has a rich blood supply, making it susceptible to hematogenous spread of bacteria, particularly from urinary tract infections, infective endocarditis, or intravenous drug use.
What are the key radiologic findings in osteomyelitis?
Early X-ray may show soft tissue swelling, while later stages reveal lytic bone lesions, periosteal elevation, and sclerosis. MRI is the most sensitive modality for early detection.
What are biofilms, and how do they contribute to chronic osteomyelitis?
Biofilms are protective bacterial communities that adhere to bone or prosthetic surfaces, resist immune clearance and antibiotics, and contribute to persistent infections.
What is the role of bone biopsy in diagnosing osteomyelitis?
Bone biopsy provides direct microbiological and histopathological evidence of infection, helping to identify the causative organism and guide antibiotic therapy.
Why is surgical debridement crucial in chronic osteomyelitis?
Chronic infections often involve necrotic bone, which lacks blood supply, making antibiotics ineffective. Surgical removal of infected tissue reduces bacterial load and prevents recurrence.
What is the difference between pyogenic and granulomatous osteomyelitis?
Pyogenic osteomyelitis is caused by pus-forming bacteria like Staphylococcus aureus, while granulomatous osteomyelitis results from chronic infections like Mycobacterium tuberculosis or fungal pathogens.
How does sickle cell anemia predispose to osteomyelitis?
Sickle cell patients experience bone infarcts due to vascular occlusion, creating an ideal environment for hematogenous bacterial seeding, particularly by Salmonella spp.
Why is septic arthritis considered a medical emergency?
Intra-articular infections cause rapid joint destruction due to inflammatory cytokines, leading to irreversible cartilage damage and loss of function if not promptly treated.
What is the pathophysiological mechanism behind septic arthritis?
Bacteria enter the synovial fluid, triggering an inflammatory response with neutrophilic infiltration, cytokine release, synovial hyperplasia, and progressive cartilage destruction.
Why is septic arthritis more common in large joints like the knee and hip?
Large joints have a greater synovial blood supply, making them more prone to bacterial seeding through hematogenous spread.
What distinguishes gonococcal arthritis from non-gonococcal septic arthritis?
Gonococcal arthritis often presents with migratory polyarthritis, tenosynovitis, and dermatitis, whereas non-gonococcal septic arthritis is more commonly monoarticular and associated with high inflammatory markers.
What are the complications of untreated septic arthritis?
Permanent joint damage, osteomyelitis, systemic sepsis, and multi-organ failure.
Why do rheumatoid arthritis patients have a higher risk of septic arthritis?
They have impaired immune function due to both the disease and immunosuppressive therapies, increasing susceptibility to bacterial infections.
What is the immune response in reactive arthritis?
Cross-reactivity between bacterial antigens (from GI or genitourinary infections) and synovial tissues leads to an autoimmune response mediated by HLA-B27.
Why is culture of synovial fluid negative in reactive arthritis?
Reactive arthritis is not caused by direct joint infection but by an immune response to a distant infection, so no bacteria are present in the joint fluid.
What are the major extra-articular manifestations of reactive arthritis?
Conjunctivitis, urethritis, mucocutaneous lesions, and keratoderma blennorrhagicum (hyperkeratotic skin lesions on palms/soles).
How does molecular mimicry contribute to rheumatic fever?
Streptococcal M protein shares structural similarities with human tissues, leading to an autoimmune attack on the heart, joints, and nervous system.
What are Aschoff bodies, and how are they related to rheumatic fever?
Aschoff bodies are granulomatous lesions found in the myocardium, characteristic of rheumatic carditis.
Why is carditis the most serious complication of rheumatic fever?
It can lead to chronic valvular damage (most commonly mitral stenosis), heart failure, and increased long-term mortality.
What is the significance of antistreptolysin O (ASO) titers in rheumatic fever?
Elevated ASO titers indicate a recent Streptococcus pyogenes infection, supporting the diagnosis of post-streptococcal rheumatic fever.
What are the five major criteria in the Jones criteria for diagnosing rheumatic fever?
Migratory polyarthritis, carditis, Sydenham’s chorea, erythema marginatum, and subcutaneous nodules.
How is chronic prophylaxis for rheumatic fever managed?
Monthly benzathine penicillin G injections are given for at least 10 years or until the patient reaches 20 years old to prevent recurrent streptococcal infections.
What distinguishes viral arthritis from bacterial arthritis?
Viral arthritis is immune-mediated and self-limited, often affecting multiple joints, while bacterial arthritis involves direct infection and requires antibiotic treatment.
How does hepatitis C virus (HCV) cause arthritis?
HCV-associated arthritis mimics rheumatoid arthritis, likely due to immune complex deposition in the joints.
What are the main differences between post-streptococcal reactive arthritis and rheumatic fever?
Post-streptococcal reactive arthritis occurs earlier, lacks carditis, and does not respond well to NSAIDs, unlike rheumatic fever.
How do arboviruses like dengue virus cause arthritis?
They trigger severe arthralgia and joint inflammation through immune complex deposition and cytokine release.
Why do immunocompromised patients have a higher risk of fungal osteomyelitis?
Fungal infections (e.g., Histoplasma, Coccidioides) are opportunistic, occurring in patients with weakened immune defenses such as HIV/AIDS or post-transplant immunosuppression.
How does osteomyelitis associated with a diabetic foot infection develop?
Diabetic neuropathy leads to unnoticed skin ulcers, which become infected, spread to underlying bone, and result in chronic osteomyelitis.
Why are Gram-negative rods like Pseudomonas aeruginosa a concern in osteomyelitis?
They are highly resistant to antibiotics and often cause osteomyelitis following puncture wounds, particularly in immunocompromised patients.
How does tuberculosis cause osteomyelitis (Pott’s disease)?
Mycobacterium tuberculosis spreads hematogenously to the spine, causing vertebral destruction, abscess formation, and spinal deformity (gibbus).
Why are immunomodulatory therapies (e.g., TNF inhibitors) associated with increased risk of osteoarticular infections?
They suppress key immune responses, reducing the body’s ability to clear bacterial and fungal infections from bones and joints.
What is the treatment strategy for multidrug-resistant osteomyelitis?
Combination therapy with prolonged intravenous antibiotics and surgical intervention to remove infected bone tissue.
