The Basketball Player With Back Pain

A previously healthy 12-year-old male resident of Winnipeg, Manitoba presented to the emergency department in March 2010 with a 2-month history of lumbar back pain and right-sided sternal chest pain exacerbated by playing basketball. His father recently noticed that he had been walking with a limp and favoring his right side. He complained of some vague, nonspecific abdominal pain but denied fever, chills, weight loss, night sweats, headaches, cough, and dyspnea. There was no history of trauma, although a similar pain was first noted in the summer of 2009 after playing dodge ball while at camp in Kenora, ON. It had promptly resolved with rest and the use of ibuprofen. The patient had immigrated to Canada in 2004. He had previously lived in Sudan and Kenya, where he had spent 2 years in a refugee camp. His father had been treated for latent tuberculosis infection in 2008. The patient was not on medications, had no animal exposures, and had not consumed unpasteurized dairy products. He had not traveled outside Canada since 2004. There were no known tuberculosis contacts. In the emergency department, he was a well-appearing adolescent with vital signs including temperature 36.5°C, pulse 83 beats/min, respiratory rate 16 breaths/min, blood pressure 112/66 mm Hg, and a normal physical examination. A radiograph done to assess his back pain revealed a right lower lobe lung consolidation as well as scoliosis (Fig. 1). Computed tomographic (CT) scan of the chest confirmed these findings and also revealed right hilar lymphadenopathy. A complete blood count revealed a white blood cell count of 9.9 × 109/L with a normal differential (6.3 × 109/L neutrophils, 2.7 × 109/L lymphocytes, 0.9x109/L monocytes, 0.1x109/L eosinophils), a hemoglobin of 12.0 g/dL, and a platelet count of 518 × 109/L The patient was referred to the pulmonary service for suspected pulmonary tuberculosis. A Mantoux test was nonreactive. Two sputum samples were collected over 48 hours for acid-fast stains and mycobacterial cultures. He was treated empirically with isoniazid, rifampin, ethambutol, and pyrazinamide.FIGURE 1.: Chest radiograph (A, PA; B, lateral) showing consolidation of the superior segment of the right lower lobe as well as a scoliosis.Two months later, the patient's symptoms had not improved, he had experienced a 15-pound weight loss, and an abscess had developed on his left thumb at the metacarpophalangeal joint. On examination, he remained well-appearing and afebrile with vital signs including temperature 36.6°C, pulse 119 beats/min, respiratory rate 18 breaths/min, blood pressure 122/81 mm Hg, and he did not show any evidence of respiratory distress. A nontender, 3-cm wide fluid collection was observed on the base of his left thumb, with normal range of motion of the joint. He had no focal spinal tenderness but had pain with lateral bending and lying flat. His neurologic examination was normal except for an antalgic gait. The 2 sputum cultures that had been obtained during his initial presentation were negative for Mycobacterium tuberculosis after 8 weeks. Repeat chest imaging showed an unchanged pulmonary infiltrate, as well as L2-L3 disc space narrowing visible on CT scan. A plain radiograph of the left hand revealed subluxation of the thumb metacarpophalangeal joint with possible associated lytic lesions (Fig., Supplemental Digital Content 1, https://links.lww.com/INF/A868). Magnetic resonance imaging of the spine revealed extensive osteomyelitis of the L1-L5 vertebrae and bilateral psoas muscle fluid collections (Fig. 2). Repeat complete blood count revealed a white blood cell count of 10.2 × 109/L with 5 × 109/L neutrophils, 3.5 × 109/L lymphocytes, 1.5 × 109/L monocytes, and 0.3 × 109/L eosinophils. His hemoglobin was 10.9 g/dL, and his platelets were 621 × 109/L. Erythrocyte sedimentation rate was 100 mm/h. A procedure was done, which determined the cause of his symptoms, and the diagnosis.FIGURE 2.: Magnetic resonance imaging of the spine showing extensive osteomyelitis from L1-L5. There was no evidence of discitis. (A, sagittal T2; B, sagittal T1).Denouement The fluid collection at the base of the left thumb drained spontaneously (Fig., Supplemental Digital Content 2, https://links.lww.com/INF/A868), and a sample was sent for Gram, fungal, and acid-fast stains, which were all negative. However, after 9 days, the fungal culture grew tan-colored colonies, which microscopically, were characterized by septate hyphae with single, short conidiophores and single conidia giving the appearance of “lollipops.” Phenotypically, the organism was highly suspicious for Blastomyces dermatitidis and this was subsequently confirmed by nucleic acid probe (AccuProbe Blastomyces dermatitidis Culture Identification Test, Gen-probe, San Diego, CA). Further investigations included an MRI of the head and upper spine, which demonstrated osteomyelitis of the odontoid and C1 vertebrae, with normal brain parenchyma and meninges. A bone scan revealed extensive disease, with additional uptake in the right mandible, left thumb and carpal bones, left distal femur and proximal tibia, and right tibia and hip. The antituberculous agents were stopped, and the patient was treated with intravenous amphotericin B deoxycholate, with good clinical response. He received amphotericin B deoxycholate 37.5 mg IV once daily for 26 days and was then transitioned to oral itraconazole at 200 mg daily. The plan is to complete at least 12 months of antifungal treatment, in accordance with the Infectious Diseases Society of America guidelines for the treatment of osteoarticular blastomycosis.1 Blastomycosis is an uncommon systemic fungal infection that is caused by the thermally dimorphic fungus, B. dermatitidis, which is endemic in the wooded areas of Manitoba, Northwestern Ontario, the Great Lakes, and the Mississippi and Ohio River Valleys.2,3B. dermatitidis exists in nature as a mold, and at body temperature as a yeast. Infective conidia become airborne when mycelia are disturbed. These conidia are inhaled into the alveoli where they enter the yeast phase.2 The clinical spectrum of B. dermatitidis infection is quite broad, ranging from asymptomatic infection to life-threatening, disseminated disease.2,4,5 Children appear to share the same clinical spectrum as adults but most commonly present with a subacute or chronic, community-acquired pneumonia unresponsive to antibiotics.5,6 Extrapulmonary disease is typically the result of hematogenous dissemination from the primary pulmonary focus, but contiguous extension from adjacent tissues is also possible.7 After lungs and skin, osseous involvement is the third most common site for blastomycosis, implicated in 6% to 48% of cases.2,3,8,9 Although any bone may be involved, the most common sites are the vertebrae, skull, ribs, and long bones.2,3,8,10 In a review of 12 blastomycosis studies that describe bone/joint disease, only 5 commented on vertebral involvement, ranging from 1.4% to 15% of all cases.8 Of the 5 children and 7 adults with vertebral blastomycosis, all had clinical or radiologic evidence of a contiguous soft-tissue abscess. Constitutional symptoms and chest radiograph abnormalities were invariably present, but ulcerative or verrucous skin lesions typical of blastomycosis were only reported in 1 patient. A review of patients in several adult hospitals in Manitoba, Canada found the most frequent manifestations of bone/joint blastomycosis were pain, soft-tissue swelling, and skin abscesses.3 Additionally, the delay between the onset of symptoms and admission was approximately 2 months, and 51% of the cases of osseous blastomycosis were initially misdiagnosed as bacterial osteomyelitis. A recent case series from our center of pediatric blastomycosis revealed 7 of 34 cases (21%) with osteoarticular involvement.6 None of the cases had vertebral disease, with involvement limited to osteomyelitis of the appendicular skeleton, the skull, and the ribs. We speculate that our patient acquired B. dermatitidis while visiting Kenora, ON during the summer of 2009. There had been no travel to Africa since 2004, which would have made the incubation period excessive. Additionally, from our review of the literature, no cases of blastomycosis have been reported from Kenya or Sudan, although a few have been reported in Rwanda, Tanzania, and Uganda.11–13 This case underscores the need to maintain a high index of suspicion for B. dermatitidis in patients with vertebral osteomyelitis and paravertebral fluid collections, particularly since vertebral tuberculosis can manifest similarly. In this case, despite the patient's exposure to an area hyperendemic for blastomycosis, the correct diagnosis was made only after there was progression of signs and symptoms while on antituberculous therapy. ACKNOWLEDGMENTS The authors thank Ms. Assunta Rendina (Health Sciences Centre, Clinical Microbiology Laboratory, Winnipeg, Manitoba, Canada) for technical assistance with this case.

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