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Infectious Disease and Microbiology – Septic Bursitis
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
Bursitis refers to inflammation of a bursa, one of more than 150 sac-like structures in the body that cushion soft tissues over bony prominences. Bursitis may result from infection (pyogenic), crystal deposition due to trauma or gout, or inflammatory arthritis such as rheumatoid arthritis. Septic bursitis most commonly involves superficial bursae and frequently affects the olecranon, prepatellar, subdeltoid, ischial, and trochanteric bursae.
The most important predisposing factor for septic bursitis is trauma, which accounts for approximately 70% of cases. Repetitive microtrauma is common in certain activities and occupations. Specific associations include ischial bursitis in individuals with spinal cord injuries, malleolar bursitis in ice skaters, and subdeltoid bursitis following injections. Additional risk factors include diabetes mellitus, alcohol abuse, chronic skin conditions, intravenous drug use, and invasive procedures such as acupuncture or joint injections, which have been associated with outbreaks of methicillin-resistant Staphylococcus aureus (MRSA).
The most common causative organism is Staphylococcus aureus. Streptococcal species account for 5–30% of cases. Gram-negative bacteria and fungi are rare causes. Prototheca wickerhamii, an environmental algae, has been reported in immunocompromised individuals. In endemic regions, brucellosis should be considered in the differential diagnosis, and tuberculous bursitis may occur as part of disseminated disease.
Clinically, septic bursitis presents with localized painful swelling, erythema, warmth, and tenderness over the affected bursa. Fever may be present. Overlying cellulitis may extend beyond the bursa. Deep bursal infections are more likely to be associated with systemic signs of infection and bacteremia.
Aspiration of bursal fluid is the diagnostic procedure of choice. Fluid analysis typically shows elevated white blood cell counts, often below 20,000 cells/mm³ in septic bursitis. Gram stain positivity varies widely, and culture of aspirated fluid has high sensitivity and specificity. Use of liquid media may improve culture yield. Crystal analysis should be performed, as crystal-induced bursitis can coexist with infection. Laboratory blood tests may show inflammatory markers, but they are nonspecific.
Imaging may support the diagnosis. Plain radiographs can demonstrate soft tissue swelling and subcutaneous edema. Ultrasound is useful in identifying fluid collections and guiding aspiration. MRI may show a fluid-filled bursa with rim enhancement after gadolinium administration, while surrounding structures are typically spared unless there is extension of infection.
The differential diagnosis includes cellulitis, fasciitis, acute monoarthritis, gout, pseudogout, and traumatic injury.
Management includes repeated needle aspiration, often daily, until the bursa is no longer fluctuant. Empiric antibiotic therapy should cover staphylococci and streptococci. For methicillin-sensitive Staphylococcus aureus, intravenous oxacillin or nafcillin is recommended. For MRSA, vancomycin is indicated. Antibiotic therapy is generally continued for at least 14 days, although shorter courses (7 days) may be sufficient in selected non-immunocompromised patients with severe infection requiring hospitalization. The choice between intravenous and oral therapy depends on severity and systemic involvement. Immobilization of the affected joint is advised during acute treatment.
If medical therapy fails, or if there is persistent swelling, pain, or loculated infection, surgical incision and drainage may be necessary. In chronic or recurrent cases, excision of the bursa may be required.
Follow-up care includes rehabilitation to prevent limitation of joint movement and ensure restoration of function.
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