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Thoracic pain that originates from thoracic spine pathology is uncommon, and it is reported to represent not more than 5% of all common spinal pain symptoms [1]. Presentations of thoracic spinal pain include “band-like” chest pain, focal pain in the mid back, and pain on deep breathing [1]. Given the paucity of primary thoracic spine pathologies, persistent thoracic pain should prompt consideration of serious conditions such as spinal infection; malignant neoplasm; traumatic or nontraumatic vertebral compression fractures; and extraspinal pathologies, such as rib fractures, peptic ulcer disease, pancreatitis, cholecystitis, pleuritis, and aortic aneurysms [1]. The incidence of infectious spondylodiskitis in developed countries is 4-24 per million each year [2]. Spondylodiskitis in adults is considered very rare; it usually follows surgical interventions or presents in cases of generalized septicemia [3]. In this report, we present a patient who described a new onset of thoracic pain that progressed without improvement, the evaluation that led to the diagnosis of coccidioidomycosis diskitis and vertebral osteomyelitis, and the course of treatment. We also discuss the diagnostic and therapeutic options and previous reports of this pathology. A 48-year-old U.S.-born white woman, who resided in the Boston area, with a known history of chronic neck pain, presented with new-onset, nontraumatic interscapular pain, and pain that encompassed the posterior left 5th-10th ribs. She denied fevers or other respiratory symptoms. Her medical history included lupus, Sjögren syndrome, chronic fatigue syndrome, depression, insomnia, fibromyalgia, and hypothyroidism. Current medications included hydroxychloroquine, cevimeline, topiramate, levothyroxine, controlled and immediate release morphine, and acetaminophen. Previously, she had taken long-term oral steroids as treatment for lupus. On examination, there was tenderness over the mid thoracic spine, and tightness of the mid thoracic paraspinal muscles bilaterally. Trunk rotation and deep breathing exacerbated symptoms. There was no muscle wasting and no deformities in the upper and lower extremities. Range of motion of the neck was reduced approximately 5% on bilateral neck rotation. Gait examination was normal to heel, toe, and tandem walking. Shoulder examination was positive for right shoulder impingement. Sensory examination to light touch, pinprick, vibration, and proprioception in the upper and lower extremities was within normal limits. Sensory testing to light touch and pinprick over the thoracic paraspinal area showed no dermatomal differences. Deep tendon reflexes were symmetric and 1+ in the upper and lower extremities, except gastroc-soleus reflexes, which were zero. The Babinski test was downgoing, there was a negative Hoffman reflex, and there was no ankle clonus. Prior imaging demonstrated spondylotic changes and an incidental 4-mm, right upper lobe nodule on cervical magnetic resonance imaging (MRI). Follow-up chest computed tomography (CT) revealed adenopathy in the superior mediastinum and a 5-mm nodule in the apex of the right lung, described by an attending radiologist as a noncalcified granuloma. The patient's presentation prompted additional evaluation with a thoracic MRI, which revealed intradiskal fluid enhancement in the T6-T7 anterior disk space, increased signal diffusely within the T6 and T7 vertebral bodies, paracentral epidural rim enhancement, and peridiskal fluid consistent with T6-T7 diskitis (Figure 1A and B). There was no evidence of cord compression or epidural abscess. (A) Magnetic resonance imaging of the thoracic spine sagittal T2 on diagnosis, demonstrating increased signal at the T6-T7 disk, endplate erosion in the anterior most part of the disk, and increased signal in the T6 and T7 vertebral bodies. (B) Axial T2 through the T6-T7 disk on diagnosis, demonstrating fluid signal in the disk space. A bone scan performed to evaluate for the presence of occult disseminated lesions demonstrated increased tracer uptake only in T6 and T7 vertebral bodies and no other active lesions. Repeated chest CT revealed no changes in the mediastinal nodes and pulmonary findings. A fluoroscopic-guided percutaneous aspirate of the T6-T7 disk space contained many white blood cells and red blood cells but no microorganisms on a Gram-stained smear. Two days after the samples were taken, a rare filamentous organism was identified; 6 days later, this organism was identified as Coccidioides posadasii/Coccidioides immitis. Treatment was promptly started with oral itraconazole. At that point, the patient was questioned about her travel history, and she reported traveling to Arizona about 8 months earlier. Within 1 month after the start of oral itraconazole, the thoracic pain worsened, and the patient developed bilateral rib pain. No fevers, chills, change in appetite, or focal upper or lower extremity weakness was reported. A neurologic examination remained unremarkable. The patient was admitted to the hospital for further evaluation, and results of laboratory studies revealed only mildly elevated erythrocyte sedimentation rate and C-reactive protein levels (37 mm/h and 1.9 mg/dL, respectively). Cultures of blood for conventional bacteria and mycobacteria yielded no growth. Repeated thoracic MRI revealed progressive destruction at T6-T7, with increased signal within the disk space, destruction of the endplates, loss of vertebral body height, effacement of the dural sac, and borderline central canal stenosis (Figure 2A and B). Given MRI findings of impeding spinal cord compromise, the patient underwent T6-T7 diskectomy, anterior interbody fusion, and posterior T3-T10 fusion using 2 fixation rods. Pathologic evaluation with periodic acid–Schiff and Gomori methenamine silver stains of the bone fragments from T6-T7 demonstrated chronic osteomyelitis and fungal elements consistent with C posadasii/C immitis infection. Antifungal treatment was switched to amphotericin B, and the patient was discharged to an inpatient rehabilitation facility in stable medical and neurologic status, with significant improvement of the rib pain. She had thoracic paraspinal pain as expected after such an extensive thoracic spinal fusion. Amphotericin B was discontinued and oral itraconazole 200 mg twice per day was prescribed for a minimum of 18 months. (A) Magnetic resonance imaging of the thoracic spine, sagittal short TI inversion recovery, 2 months after diagnosis, demonstrating significant increased signal in the T6-T7 disk with endplate erosion, vertebral body collapse, and spinal cord compression. (B) Axial T2 through the T6-T7 disk, demonstrating significant intradiskal fluid enhancement and epidural enhancement. Coccidioidomycosis is a fungal infection caused by C posadasii/C immitis, pathogens that are prevalent in arid regions of the southwestern United States, Mexico, and Central and South America. This infection is also known as San Joaquin Valley fever. Coccidioidomycosis typically is transmitted by inhalation during dry seasons, or when the soil is disturbed and thus made airborne [4, 5]. Most patients exposed to coccidioidomycosis remain asymptomatic, but hypersensitivity symptoms can occur 7-21 days after infection [6, 7]. The most common initial presentation of a coccidioidomycosis infection is pneumonia, and symptoms manifest as fever, cough, chest pain, fatigue, night sweats, headache, arthralgias, and myalgias. These symptoms are usually self-limited [7]. Extrapulmonary spread occurs in less than 1% of the population and potentially involves any organ system [7]. The mechanism is thought to be hematogenous from the pulmonary venous system [5, 7]. Hematogenous spread explains unifocal or multifocal [8] spinal involvement in the cervical, thoracic, and lumbar levels. Lymphatic spread also can occur, because coccidioidomycosis pneumonia is associated with hilar adenopathy and lymph node involvement [5]. Risk factors for dissemination include an immunocompromised state [5]. It is possible that this patient's prior use of oral corticosteroids increased her risk of infection. To further explore the initial presentation patterns in coccidioidomycosis spinal infections, we reviewed 4 published case reviews, which contained a total of 33 patients, including 11 detailed case reports that contained presenting histories [9-12] (Table 1). Of these 11 patients, 6 presented with the typical constitutional symptoms of fever, weight loss, chest pain, and cough [9-12]. In these 6 cases, subsequent development of back pain spurred investigation, which revealed dissemination to the spine. Of the remaining cases, presentations were the following: 2 patients with foot lesions and back pain [9, 11], 1 patient with cutaneous lesions and back pain [9], and 1 patient with cutaneous lesions and clavicular pain [9]. Diagnosis was made after foot or skin biopsies. In all of these cases, after the initial presentation, imaging of the chest and spine revealed spinal involvement. The last case reviewed was a patient who presented with a paraesophageal mass; imaging revealed multiple foci in the skull, clavicle, and cervical spine [10]. By contrast, our patient's presentation appears to be atypical, because she initially presented solely with thoracic spinal pain (assuming that the neck pain was unrelated), and there was no radiographic evidence of coccidiomycosis in the lungs or in other organs. The pulmonary lesions identified on CT were radiologically not related to coccidioidomycosis. However, we do not have pathology confirmation because these nodes were not biopsied due to the lack of changes on repeated CT. It is worth noting that only 1 of the 33 patients included in the 4 case reviews was not a permanent resident of the Southwest region [12]; this patient had acquired coccidioidomycosis only after visiting Arizona, similar to our patient. Because coccidioidomycosis is endemic to the Southwest region, it should be considered in patients who have traveled to or are former residents of this region. Conventional radiography in suspected coccidioidomycosis diskitis and vertebral osteomyelitis is likely to reveal erosive defects and sclerosis in vertebral endplates [10]. Also, disk height usually is preserved in coccidioidomycosis diskitis and vertebral osteomyelitis, except in late disease [9, 10]. Anterior and posterior elements of the vertebral body may be involved, which lead to bony destruction and vertebral collapse as the disease progresses [11]. CT will demonstrate involvement of vertebrae and endplates and is useful for delineating the extent of bony destruction for planning biopsies or surgery. Nevertheless, as is the case with conventional radiography, CT has low sensitivity for early disease detection [7, 11]. MRI is most sensitive for identifying early coccidioidomycosis diskitis and vertebral osteomyelitis [8, 11, 13]. Features are variable, but foci usually appear as disk space signal changes and heterogeneous changes in vertebral body marrow [8]. Lesions are of low signal on T1-weighted sequences and of bright signal on T2-weighted and short TI inversion recovery sequences, due to inflammatory edema and replacement of marrow fat [8, 14]. On postcontrast imaging, there may also be enhancement in the disk space, vertebral bodies, and adjacent soft tissues caused by hyperemia in acute inflammation. Follow-up MRI and radiographs are reviewed to evaluate the involved sites and non–abscess-forming extensive spread into paravertebral soft tissues, including the neural contents in advanced disease [8, 11]. Bone scintigraphy is usually positive within 1-2 days of symptom onset and shows increased uptake in vertebral bodies and adjacent involved bone [8, 14]. A bone scan is useful in screening for disseminated lesions [8, 11]. In our patient, a bone scan revealed uptake only in the thoracic spine. Laboratory studies in suspected infectious spondylitis and diskitis can reveal elevated erythrocyte sedimentation rate and C-reactive protein in patients who are not immunocompromised; elevations of both values were mild in our patient, notwithstanding that she was receiving treatment for systemic lupus. Immunoglobulin M antibodies are prevalent in acute disease, usually 1-3 weeks after symptom onset, and immunoglobulin G is prevalent in chronic disease, as early as the second week to as late as the 28th week of symptom onset [6, 15]. Serology titers higher than 1 in 16 may indicate disseminated disease, and higher than 1 in 128 may indicate bone and joint disease [6]. Initial treatment of fungal spondylodiskitis requires the correct identification of the pathogen. Fluoroscopic or CT-guided transpedicular vertebral and disk biopsies are effective methods to obtain a pathogen for identification [16]. Specimens can be identified as C immitis or C posadasii by direct hematoxylin-eosin (Figure 3A) or periodic acid–Schiff stains in just 2 days [8]; more sensitive and specific stains are calcofluor white fluorescent stain and Gomori methenamine silver preparations [15] (Figure 3 B). (A) A section of vertebral bone, demonstrating fungal osteomyelitis. The spherules are visible with routine staining and are surrounded by a pyogenic reaction that may be the result of spherule rupture and release of endospores (hematoxylin-eosin, original magnification ×400). (B) Mature spherule containing endospores (Gomori methenamine silver, original magnification, ×1000 oil immersion). First-line medical management of disseminated coccidioidomycosis is azole therapy, which includes oral itraconazole, fluconazole, and posaconazole. Itraconazole is preferred in spondylodiskitis because of its better bone penetration [17]. Intravenous azole therapy can be loaded for several days in a patient who is unstable, followed by oral therapy. The recommended minimum course of oral therapy is 12-18 months from the moment the patient shows a response to the treatment, such as declining serum anticoccidioidal titers [17]. High-dose fluconazole (400-1000 mg intravenously or orally daily) is preferred for meningitis because of this antifungal's superior cerebral spinal fluid penetration. Amphotericin B is preferred in pregnancy and for lesions in critical locations, such as within the spinal canal. Amphotericin B also is preferred if first-line treatment with an azole fails. Intrathecal amphotericin B may be required for meningitis if the response to an azole is poor. Lifelong treatment with an azole is recommended for the patient with meningitis and for the patient who is immunocompromised and with disseminated coccidioidomycosis [17]. Surgery is warranted in cases of progressive infection, abscess formation, osteolysis, neurologic compromise, or intractable pain [18-20]. Anterior and posterior surgical approaches for decompression and fusion can vary, depending on the location of infection; but the ultimate goals are to preserve neurologic function and spine stability, and to eradicate infection [20]. It is demonstrated that, in coccidioidomycosis bone infections, the combination of surgical and medical treatment is more effective than each treatment alone [11, 21]. Twenty-four of the 33 cases included in our literature review ultimately required surgical debridement to address spinal cord compromise (n = 8), vertebral instability, or recurrence of infection. This case emphasizes the importance of properly investigating thoracic pain, especially if the patient has persisting symptoms despite conservative treatment [22]. There are indications in the literature that complicated fungal diskitis and vertebral osteomyelitis usually require surgical and medical treatment. This will require further studies for evaluation of both treatment modalities alone or in combination. Given the relative infrequency with which coccidioides diskitis and vertebral osteomyelitis occur, case report literature and expert opinion will likely remain the basis of diagnostic and treatment algorithms. As demonstrated in this case patient who had previous diagnoses of chronic cervical pain and fibromyalgia and a lack of initial “red flags,” suspicion was raised only when she did not experience relief from conservative treatment. Teamwork from interventional spine physiatry, skilled spine surgery, and prompt infectious disease management was necessary for treatment of this unusual spine pathology. Recent improvements in imaging technology and a high index of suspicion may reduce the need for surgery for future patients. We thank Todd E. Abbott, MD, director, Cytopathology Commonwealth Pathology, Partners Newton-Wellesley Hospital, Newton, Massachusetts, for his help in furnishing the pathology slides.