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Candida albicans lumbar spondylodiscitis in an intravenous drug user: a case report

Background Spondylodiscitis leads to debility, and few data exist on Candida spondylodiscitis in patients with intravenous drug use. Case presentation We present a case of Candida albicans lumbar spondylodiscitis in a patient with intravenous drug use. This patient was treated with surgical debridement and 9 months of fluconazole therapy, and the neurological deficits resolved completely. The infection did not recur clinically or radiologically during 9 months of follow-up. Conclusion Although Candida albicans lumbar spondylodiscitis is rare, Candida should be suspected as a causative pathogen in patients with intravenous drug use except for Staphylococcus aureus, Pseudomonas aeruginosa, and Mycobacterium tuberculosis. As soon as Candida albicans lumbar spondylodiscitis is suspected, magnetic resonance imaging and percutaneous biopsy should be performed. Surgical intervention combined with treatment with antifungal medications can successfully eradicate the infection and resolve the neurological deficits.


Background
Spondylodiscitis is a rare disease accounting for 2-7% of all cases of pyogenic osteomyelitis, with incidence varying from 1 per 100,000/year to 1 per 250,000/year [1,2]. However, the incidence of spondylodiscitis is rising because of longer life expectancy and more patients with chronic debilitating disease, use of immunosuppressive therapy, increasing use of indwelling devices, and spinal surgery [3][4][5].
The first patient with fungal Monilia psilosis osteomyelitis was reported by Connor in 1928 [6], and there was no report of Candida osteomyelitis in the literature until 1970 [7]. A study by Gathe et al. showed that approximately 60% of cases of Candida osteomyelitis occur in the spine [8]. Few data exist on Candida infection in patients with intravenous drug use (IVDU) [9][10][11]. We report on a case of Candida albicans lumbar spondylodiscitis (CaLS) in a patient with IVDU, including the clinical presentation, radiological findings, and outcome of combined surgical and medical treatment after 9 months of follow-up.

Case Presentation
A 41-year-old man with a history of IVDU with injection of heroin initially presented to our clinic with a 3-month history of lower back pain radiating to the lower limbs bilaterally. Findings on neurological examination were normal, and he was treated with oral non-steroidal antiinflammatory drugs. Three months later, he developed myelopathic symptoms with weakness of both lower limbs and severe back pain and presented to the neurosurgery clinic of our institute. Magnetic resonance imaging (MRI) of the lumbar spine showed diffuse bone marrow infiltration plus endplate erosion level at L3 and L4 characterized by low signal intensity on a T1-weighted image and high signal intensity on a T2-weighted image, with enhancement in affected bodies and cystic enhanced lesions in the epidural and paraspinal regions after administration of gadolinium ( Figure 1). Radiologically, pyogenic discitis, vertebral osteomyelitis, and epidural and paraspinal abscesses had to be considered. The patient was treated with oral non-steroidal anti-inflammatory drugs at the clinic. On examination, there was generalized weakness of grade 4 in related muscle groups and positive myelopathic signs in the lower extremities. The initial laboratory findings revealed an elevated erythrocyte sedimentation rate (ESR) (98 mm/hr; normal range, <10 mm/hr) and anemia (12.3 g/dL; normal range, 14-17 g/dL). However, the results of other laboratory tests were within normal limits, including the white blood cell count (12,500 cells/mm 3 ).
Radiography of the lumbar spine revealed spondylosis of the lumbar spine with osteophyte formation and decrease disc height at L3-4. The patient underwent surgery for symptomatic relief; left laminotomy over L3, discectomy over L3-4 under a microscope, and debridement of the disc and endplate were performed and showed necrotic debris and fluid accumulation in the L4-5 disc and endplates as well as a disc bulging over the L3-4 level. The patient was treated empirically with intravenous cefuroxime and gentamycin until candidal infection was confirmed 3 days later. The clinical diagnosis was CaLS, and the patient was subsequently treated with intravenous fluconazole 400 mg/day for 6 weeks and then oral fluconazole 300 mg/day for another 3 months. Nine months later, the patient's ESR was 8 mm/hr; he had recovered from his neurological deficit with complete return of motor function in the lower limbs and was walking normally, and the motor weakness and pain in his legs had resolved completely. Serial follow-up radiographs after surgery and MRI showed significant shrinkage of the vertebral osteomyelitis, discitis, and paraspinal abscesses ( Figure 2), although there were still abnormal signal and enhanced lesions in the disc adjacent to the affected vertebral bodies. The patient recovered very well during the 9-month follow-up period and does not have human immunodeficiency virus infection. This is the first report of CaLS in a patient with IVDU. Although Candida species are low-virulence organisms that inhabit the skin and mucous membrane of humans, the incidence of disseminated and deep-seated Candida infections in patients with IVDU is increasing [9][10][11][12][13]. A new pattern of spondylodiscitis in IVDU is emerging, characterized by more frequent unusual pathogen involvement, a severe clinical course, and a need for surgery. Our patient was treated with surgical debridement and antifungal medications.
There are no non-invasive diagnostic tests or typical radiological findings in CaLS. Reports by Waldvogel and Gathe showed that the delay in diagnosis between the onset of symptoms and the diagnosis of CaLS ranges from 1 month to several years, with an average of 3.3 months [7]. Symptoms such as low-grade fever, malaise, and weight loss are non-specific. Similarly, anemia, neutrophilia, and elevated ESR are also non-specific, representing a chronic inflammatory process, although a markedly elevated ESR is suspicious of infection.
Candida spondylodiscitis usually involves the intervertebral disc space with narrowing of the disc cartilage, causing destruction and lysis of the vertebral endplates and underlying vertebral bone [8]. The findings on MRI include an absence of disc hyperintensity and preservation of the internuclear cleft on T2-weighted images in addition to increased signal intensity on gadoliniumenhanced T1-weighted images and early disc destruction and paraspinal abscesses [15]. The delay of antifungal medical or surgical treatment in our case allowed us to evaluate the natural course of the disease. Candida affects the spinal segments probably through hematogenous dissemination, and once a focus develops in the vertebral body, it continues an indolent course [12]. In our case, vertebral collapse, psoas abscess formation, and neurological deficits became apparent within 3 months of the onset of symptoms. The reasons for delayed suspicion and diagnosis in our case included a delay in presentation and a delay of investigation. A high index of suspicion and immediate MRI would have confirmed the pathologic lesions before vertebral collapse and neurological compromise developed. As soon as lumbar spondylodiscitis is suspected, MRI and percutaneous biopsy should be performed, followed by medical therapy. This may halt the progression of bony destruction and prevent the need for surgical treatment [16]. Surgery is primarily indicated for failure of or relapse after conservative treatment, significant spinal collapse, and neurological deficits [17].
The management of patients with CaLS includes conservative treatment with biopsy, medical therapy, and bed rest; posterior surgical stabilization and transpedicular biopsy with or without fusion; or anterior debridement of the abscesses, tissue diagnosis, and fusion combined with posterior stabilization. Some investigators have recommended primary reconstruction for all pyogenic infections of the spine to maximize eradication of the infection [18], and others have recommended surgery to aid in diagnosis as well as decompression and stabilization of the spine at the same time [19]. Combined debridement and treatment with an antifungal agent was performed in this case because there is controversy regarding the use of instrumentation in the presence of infection, and in this case the infection was successfully eradicated and the neurological deficits were resolved.

Conclusions
Although CaLS is rare, Candida should be suspected as a causative pathogen in patients with IVDU except for Staphylococcus aureus, Pseudomonas aeruginosa, and Mycobacterium tuberculosis. Without adequate treatment, the disease is progressive and leads to vertebral destruction and spinal cord and neural compression. Early recognition of CaLS may be difficulty until the patient either develops back pain with symptoms of impending cord compression or develops various grades of neurological deficits. As soon as CaLS is suspected, MRI and percutaneous biopsy should be performed, followed by medical therapy. This may halt the progression of bony destruction and prevent the need for surgery. However, if vertebral collapse and spinal cord compression occurs, surgical intervention combined with antifungal therapy can successfully eradicate the infection and resolve the neurological deficits.