Case Presentation: A 46 year-old gentleman presents with an acute worsening of his chronic low back pain with radiation and paresthesias down his left leg. On admission, he was febrile, tachycardiac and uncomfortable appearing. He has point tenderness of lumbar spine, normal rectal tone, 2+ patellar, Achilles reflexes and 5/5 strength in bilateral upper and lower extremities. CT spine demonstrated L4-L5 discitis and vertebral osteomyelitis with left psoas abscess extending to the epidural space with and narrowing of spinal canal. ESR was elevated at 55 mm/hr and CRP was 1.6 mg/dL; blood cultures were negative. He was empirically started on vancomycin and cefepime. Further questioning revealed no recent surgical intervention, open wounds or history of IV drug use. Neurosurgery was consulted and deferred acute surgical intervention; bone biopsy was obtained on hospital day two and cultures returned negative. Following nine days of IV antibiotic therapy, patient was discharged on oral trimethoprim-sulfamethoxazole and ciprofloxacin with outpatient neurosurgery and infectious disease follow-up. One month later, he presented with worsening back pain, intermittent fevers, inability to perform activities of daily living and new loss of sensation over his left lateral thigh. Repeat imaging showed progression of abscess and osteomyelitis. Vancomycin and cefepime were re-initiated and interventional radiology drained psoas abscess. Cultures were, once again, negative. Neurosurgery deferred surgical intervention to the outpatient setting and he was discharged on ceftriaxone and vancomycin. He underwent washout and laminectomy, two months after the initial presentation. Surgical cultures were positive for Burkholderia cepacia – resistant to ciprofloxacin and intermediate sensitivity to cefepime.
Discussion: Burkholderia cepacia complex is a group of nine species of aerobic, gram-negative bacilli found in water, soil and plants. The pathogenicity in humans is usually observed in patients with cystic fibrosis. It is also a colonizer and has caused hospital outbreaks associated with IV fluids, contaminated detergents and transducers. Our microbiology laboratory was able to verify that that Burkholderia cepacia was not isolated from any other cultures at that time to suggest contaminant, an outbreak or hospital associated source of infection. Reports of skin and soft tissue infections and osteomyelitis usually have an indolent course and are seen in IV drug users, post operatively or with indwelling catheters. Our patient had none of these exposures at the time of presentation, which has only been reported once in the literature. Burkholderia cepaciais is commonly resistant to beta lactams and aminoglycosides, often leading to failure of empiric therapy. They are usually susceptible to trimethoprim-sulfamethoxazole, carbapenems and tetracyclines.
Conclusions: We present a case of vertebral osteomyelitis due to Burkholderia. It is unclear if Burkholderia cepacia was the only pathogen given the delay in debridement and cultures; however our patient had an indolent course, which is commonly seen in Burkholderia cepacia infections. Initial treatment with trimethoprim-sulfamethoxazole should have been appropriate antimicrobial therapy, but the nidus of infection was not removed with early surgical intervention. This case emphasizes the importance of early source control and cultures to guide extended antibiotic therapy in osteomyelitis.