Infectious disorders

Osteomyelitis

It is an inflammation of the bone caused by a pyogenic organism. Depending on the timeline of disease onset, osteomyelitis may be acute (presenting within two weeks of infection), subacute (presenting within a few weeks to months) or chronic (presenting in a few months). It may be caused by hematogenous dissemination of an infection especially in children and elderly; or it may follow injury to bone and adjoining soft tissues from trauma or surgery. Prosthetic joint devices, diabetes mellitus and sickle cell disease are common risk factors for osteomyelitis. Acute osteomyelitis in children tends to affect the metaphysis of long bones of the extremities. Vertebral and hip joint involvement is more common in adults. Clinical presentation includes fever, malaise, bone pain and tenderness, erythema, swelling, decreased range of motion and purulent discharge in some cases. Some patients may have minimal symptoms. Foul smelling pus discharge occurs in anaerobic infections.

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 the diagnosis of osteomyelitis. X-ray has a low sensitivity and may be negative in the early stages. Radiography findings include necrotic bone tissue or sequestrum surrounded by sclerotic bone or involucrum. Blood cultures may be positive. Bone scintigraphy or bone scan using radioactive technetium-99, MRI, CT and radiolabelled white blood cell scan have increased sensitivity and specificity to diagnose osteomyelitis. Ultrasound is helpful especially in situations where radiation exposure is undesirable. Treatment should be guided by the causative organism and is continued for at least 4-6 weeks. At least initially, parenteral antibiotics are preferred. Some cases may need surgical debridement and removal of necrotic bone.

Septic arthritis

It is inflammation of the joint caused by infectious agents and involves the synovial space. Bacteria are the most common cause of septic arthritis and 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. Hematogenous seeding during a septicaemia or bacteremia is the most common route of infection. Patients with degenerative joint disease, rheumatoid arthritis and those on corticosteroid therapy are at higher risk of septic arthritis. Bacterial invasion of the joint synovium incites an acute inflammatory response with neutrophils and phagocytes. Bacterial toxins, enzymes and pro-inflammatory cytokines like interleukin-1 and tumor necrosis factor-alpha lead to destruction of the synovium and articular cartilage. Clinical features include fever, joint pain and swelling, reduced range of motion affecting most commonly the large joints like the knee and hip joints. Gonococcal septic arthritis tends to be polyarticular with migratory polyarthritis and tenosynovitis. Gold standard for diagnosis is microscopy and culture of the synovial fluid which 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 that has accumulated in the joint space is needed in many cases.

Reactive arthritis

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

Necrotizing fasciitis

Also known as “flesh eating disease”, is a rare and potentially fatal infection of the fascia and subcutaneous tissues. It follows minor trauma like cuts, scrapes, insect bites, intravenous injections, acupuncture etc. and sometimes surgery, burns and childbirth. Infection starts in the deep tissues and spreads along fascial planes, causing gangrene in severe cases. Endotoxins and exotoxins secreted by infecting bacteria cause tissue damage. Toxic shock syndrome may occur in some cases.

Presenting signs and symptoms include local erythema, pain out of proportion to the inflammation and involving non-inflamed areas, fever, tachycardia, sepsis, shock, altered sensorium, local bullae, necrosis and organ failure. Lymphadenitis and lymphangitis are characteristically absent. It is called Fournier gangrene when infection involves the perineum and Ludwig angina when infection involves the submandibular and sublingual spaces.

Depending on the type of microbes involved, necrotizing fasciitis can be classified as type I and 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 is key to avoid life-threatening complications from necrotizing fasciitis. Biopsy and Gram stain will demonstrate infectious organisms. Other lab findings include leukocytosis, thrombocytopenia, and azotemia. Computed tomography (CT) scanning or magnetic resonance imaging (MRI) can detect subcutaneous and fascial edema or tissue gas (“gas gangrene”). Investigations should never delay treatment when the clinical suspicion is high. Once group A Streptococcus is confirmed to be the etiology, high dose penicillin or ampicillin and clindamycin (which interferes with toxin production) should be given. 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 cases of severe necrotizing fasciitis.