Infectious disorders

Osteomyelitis

Osteomyelitis is inflammation of bone caused by a pyogenic organism. Based on the timing of presentation, osteomyelitis may be:

• Acute: presents within 2 weeks of infection
• Subacute: presents within a few weeks to months
• Chronic: presents after a few months

Infection may reach bone through:

• Hematogenous spread (especially in children and older adults)
• Direct inoculation after trauma or surgery involving bone and adjacent soft tissue

Common risk factors include prosthetic joint devices, diabetes mellitus, and sickle cell disease.

Typical sites of involvement:

• Children (acute osteomyelitis): metaphysis of long bones of the extremities
• Adults: vertebrae and hip joint involvement is more common

Clinical presentation may include fever, malaise, bone pain and tenderness, erythema, swelling, decreased range of motion, and (in some cases) purulent discharge. Some patients have minimal symptoms. Foul-smelling pus suggests anaerobic infection.

Microorganisms causing osteomyelitis

• Most common cause of acute hematogenous osteomyelitis - S.aureus, followed by S.epidermidis, E.coli, Pseudomonas aeruginosa and Serratia marcescens
• Sickle cell anemia - Salmonella and S.pneumoniae
• Immunocompromised patients - Candida albicans and Aspergillus spp.
• Orthopedic implants - coagulase negative Staphylococci like S.epidermidis
• Diabetes mellitus - polymicrobial infection with aerobes and anaerobes
• Foul smelling pus - anaerobes

Bone biopsy is the gold standard for diagnosing osteomyelitis.

• X-ray has low sensitivity and may be negative early in the disease.
• Radiographic findings can include necrotic bone tissue (sequestrum) surrounded by sclerotic bone (involucrum).
• Blood cultures may be positive.
• Imaging tests with higher sensitivity and specificity include bone scintigraphy (bone scan) using radioactive technetium-99, MRI, CT, and radiolabelled white blood cell scan.
• Ultrasound can be helpful, especially when radiation exposure is undesirable.

Treatment should be guided by the causative organism and continued for at least 4-6 weeks. Parenteral antibiotics are preferred initially. Some cases require surgical debridement and removal of necrotic bone.

Septic arthritis

Septic arthritis is inflammation of a joint caused by infectious agents and involves the synovial space. Bacteria are the most common cause, and the likely etiology varies by age group.

• In young adults, Neisseria gonorrhoeae causes the majority of infections.
• In other age groups, S.aureus, H.influenzae, Streptococci, and Gram negative bacteria are more common.

The most common route of infection is hematogenous seeding during septicemia or bacteremia.

Higher-risk groups include patients with degenerative joint disease, rheumatoid arthritis, and those on corticosteroid therapy.

Pathogenesis: bacterial invasion of the synovium triggers an acute inflammatory response with neutrophils and phagocytes. Bacterial toxins, enzymes, and pro-inflammatory cytokines (including interleukin-1 and tumor necrosis factor-alpha) contribute to destruction of the synovium and articular cartilage.

Clinical features include fever, joint pain and swelling, and reduced range of motion. Large joints (especially the knee and hip) are most commonly affected. Gonococcal septic arthritis tends to be polyarticular, with migratory polyarthritis and tenosynovitis.

The gold standard for diagnosis is microscopy and culture of synovial fluid. Synovial fluid typically shows a predominantly neutrophilic infiltrate with counts > 50,000/mm³.

Systemic antibiotic therapy is the mainstay of management and is guided by age and microbiology. Typically, third generation cephalosporins are used. Drainage of pus from the joint space is needed in many cases.

Reactive arthritis

Reactive arthritis is a non-infectious arthritis associated with certain microbes.

Necrotizing fasciitis

Necrotizing fasciitis (also called “flesh eating disease”) is a rare, potentially fatal infection of the fascia and subcutaneous tissues. It may follow minor trauma (cuts, scrapes, insect bites, intravenous injections, acupuncture) and can also occur after surgery, burns, or childbirth.

The infection begins in deep tissues and spreads along fascial planes, causing gangrene in severe cases. Endotoxins and exotoxins produced by the infecting bacteria contribute to tissue damage. Toxic shock syndrome may occur.

Presenting signs and symptoms include local erythema, pain out of proportion to the visible inflammation (often extending into non-inflamed areas), fever, tachycardia, sepsis, shock, altered sensorium, local bullae, necrosis, and organ failure. Lymphadenitis and lymphangitis are characteristically absent.

Special terms based on location:

• Fournier gangrene: infection involves the perineum
• Ludwig angina: infection involves the submandibular and sublingual spaces

Depending on the microbes involved, necrotizing fasciitis is classified as type I or type II. Type II necrotizing fasciitis is also known as hemolytic streptococcal gangrene. Some cases are caused by Vibrio vulnificus.

Prompt diagnosis and management with intravenous antibiotics and surgical debridement are key to avoiding life-threatening complications. Biopsy and Gram stain can demonstrate infectious organisms.

Other lab findings include leukocytosis, thrombocytopenia, and azotemia. CT scanning or MRI can detect subcutaneous and fascial edema or tissue gas (“gas gangrene”). Investigations should never delay treatment when clinical suspicion is high.

Once group A Streptococcus is confirmed as the etiology, give high-dose penicillin or ampicillin plus clindamycin (which interferes with toxin production). Vancomycin, clindamycin, and piperacillin/ tazobactam or linezolid and piperacillin/tazobactam are effective regimens for all cases. Imipenem or meropenem can be used instead of piperacillin/tazobactam. Intravenous immunoglobulin may be considered in severe cases of necrotizing fasciitis.