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Clinical Infection & Immunity

Case Report

Volume 4, Number 1, March 2019, pages 12-15

A Rare Case of Primary Spinal Epidural Abscess Caused by Streptococcus mitis in an Immunocompetent Adult With Incidentally Diagnosed Allergic Bronchopulmonary Aspergillosis

A spinal epidural abscess (SEA) is a rare suppurative infection of the epidural space that can mechanically compress the spinal cord. Bacteria gain access to the epidural space hematogenously, by direct extension, or via direct inoculation into the spinal canal. SEA is almost always associated with risk factors, such as diabetes, human immunodeficiency virus (HIV), malignancy, chronic renal insufficiency, intravenous (IV) drug use, recent dental surgery, or spinal injections [1, 2]. Staphylococcus aureus is the most commonly implicated organism [2]. Diagnosis is made by magnetic resonance imaging (MRI) or, if unavailable, computed tomography (CT) with contrast. Surgical decompression and drainage with systemic antibiotic therapy is the treatment of choice for most patients, particularly for those with acute neurological deficits.

Our patient is a middle-aged woman who presented to the emergency room with 1-week history of low back pain which began insidiously, with no known trauma or inciting event. It was in the lumbar area, just left of the midline, and was associated with intermittent shooting pain radiating down the back of the left leg to the left knee. She had no fever or chills. Her most recent dental procedure was dental cleaning 6 months ago. She had no history of epidural injections or spinal surgery, and had never used IV drugs. Her medical history was significant for asthma and allergic symptoms. On presentation, she was hypoxic to 87% on room air, but otherwise hemodynamically stable and afebrile. Physical exam was notable for diffuse expiratory wheezing, and tenderness to palpation over the lumbar spine. She had none of the red-flag signs of spinal cord compression. Initial laboratory testing revealed a macrocytic anemia with hemoglobin of 11.3 g/dL, a normal white blood cell count of 7.1 × 10³/uL with 60% neutrophils and 28% lymphocytes. D-dimer was mildly elevated at 1.35. Her arterial blood gases on 2 L of supplemental oxygen revealed a normal pH of 7.41, with a pO₂ of 87 mm Hg and a pCO₂ 40 mm Hg. The hypoxia prompted a chest X-ray which revealed bilateral patchy opacities suggestive of multifocal pneumonia, and she was started on oral moxifloxacin. A CT pulmonary angiogram ruled out pulmonary thromboembolism, and demonstrated patchy ground-glass opacities associated with air bronchograms in both lungs with predominance in upper lobes and peribronchial distribution (Fig. 1). MRI of the lumbar spine with and without contrast revealed a multiseptated fluid collection in the posterior epidural space, measuring 5.5 × 1.7 × 0.8 cm (craniocaudal, transverse and anteroposterior) extending from L1 to L3 level, with moderate to marked central canal stenosis at L1-L2 and L2-L3 levels (Fig. 2). There was no intradural or meningeal enhancement noted. Blood cultures were not drawn as she had already been started on oral antibiotics for suspected pneumonia. The antibiotic regimen was switched to IV vancomycin and cefepime. The patient required supplemental oxygen by nasal cannula, and continued to have expiratory wheezing. She was treated with albuterol-ipratropium nebulization, and was started on a course of oral prednisone for acute exacerbation of asthma. The epidural abscess was aspirated under fluoroscopic guidance, and its contents were yellow and turbid. Cytology of the aspirate showed degenerating acute neutrophilic exudate, and was negative for malignant cells. Culture of the aspirate had moderate growth of Streptococcus mitis, which was resistant to only erythromycin. The neurosurgery service was consulted, but did not recommend surgical decompression, as the patient was improving after abscess aspiration with antibiotics alone. The patient was monitored with frequent neurological exams for signs and symptoms of cord compression, which she did not develop. She had an episode of cough with hemoptysis, and epistaxis. Further lab investigation revealed high immunoglobulin E (IgE) levels (4,030 U/mL), and antibody testing for Aspergillus fumigatus showed a high IgE titer of 2.96 kU/L, and negative IgG titer of 4.09 U/mL. Respiratory viral panel was negative. She was diagnosed to have acute allergic bronchopulmonary aspergillosis (ABPA) for which she was started on itraconazole. Transthoracic and transesophageal echocardiograms ruled out infective endocarditis (IE) as a potential source of hematogenous spread to the epidural space. C-reactive protein was elevated at 20.4 mg/dL and trended down to 8.1 mg/dL after 4 days of treatment. Other acute phase reactants erythrocyte sedimentation rate and ferritin were both high at 76 mm/hr and 817 ng/mL, respectively; however these values were obtained after 4 days of treatment. Her HIV antigen/antibody screen was negative. Notably, not only was she immunocompetent, but she could even be considered hyperimmune as evidenced by the incidental finding of acute ABPA, which is a complex hypersensitivity reaction. She did not have any of the risk factors associated with SEA too. She was discharged with a peripherally inserted central catheter for administering 6 weeks of IV ceftriaxone 2 g daily. Repeat imaging by non-contrast MRI 5 weeks later showed interval decrease in size of the epidural fluid collection and resolution of the mass effect on the thecal sac (Fig. 3).

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Figure 1. Computed tomography pulmonary angiogram. Patchy ground-glass opacities are seen in both lungs, associated with air bronchograms, with predominance in upper lobes and a peribronchial distribution. This is suggestive of either multifocal pneumonia, or an inflammatory process.

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Figure 2. Magnetic resonance imaging of the lumbar spine with contrast. A multiseptated fluid collection is seen in the posterior epidural space, measuring 5.5 × 1.7 × 0.8 cm (craniocaudal, transverse, and anteroposterior), extending from L1 to L3 level, with moderate to marked central canal stenosis at L1-L2 and L2-L3 levels, with no intradural or meningeal enhancement.

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Figure 3. Magnetic resonance imaging of the lumbar spine without contrast. Imaging obtained 5 weeks after initiating antibiotics showed interval decrease in size of the epidural fluid collection and resolution of the mass effect on the thecal sac.

SEA is a rare but serious infection which requires a high suspicion for diagnosis, because of the non-specific symptoms, as well as its rarity: a case series of 101 cases estimated the incidence of SEA to be around 5.1 per 10,000 hospital admissions [1]. SEA occurs in all age groups, and is more commonly seen in men [2]. The rising incidence of SEA may be attributed to both a growing number of patients with predisposing factors, and wider availability of neuroradiological imaging techniques [1, 3]. In the majority of cases, bacteria reach the epidural space by hematogenous dissemination, where the primary sources are skin, respiratory tract, and bloodstream [1, 4]. Less commonly, SEA develops by contiguous spread from adjacent tissues such as vertebral osteomyelitis, discitis, or paraspinal abscess. In a meta-analysis of 915 patients [2], risk factors and infection sources could be identified for 854 patients in the literature, many of whom had more than one risk factor or potential source of infection. Of the 854 patients, diabetes was the most commonly observed comorbidity, affecting 14%, followed by IV drug use and alcohol abuse. A source of infection was identified in 44%, of whom skin abscesses were most common. In 22% of patients, invasive procedures were implicated as the cause of SEA, including epidural and spinal anesthesia, extraspinal and spinal surgery, paravertebral injections, and less commonly epidural injections, lumbar punctures and dental extraction.

SEA is primarily a bacterial infection, and Staphylococcus aureus is the principal agent implicated, responsible for up to 73% of SEA cases [1, 2, 4, 5]. Less common agents are Staphylococcus epidermidis (in patients with spinal procedures, catheters, anesthesia, or surgery), gram-negative bacilli (Escherichia coli from urinary source, Pseudomonas aeruginosa (in injection-drug users)), Streptococci, and anaerobes [2, 6]. Parasites and mycobacteria are very rare causes of SEA, and are limited to geographic areas [2, 6]. While Streptococcus mitis is a leading cause of IE among the oral Streptococci, to our knowledge, there have only been two previous reported instances of SEA in association with Streptococcus mitis IE [7, 8].

Back pain and fever are frequent initial symptoms, occurring in 71% and 66% of the patients respectively in the meta-analysis [2]. The second stage is marked by radicular irritation, and the development of neurological deficits heralds the third stage. In the fourth and final stages, paralysis affected 34% of patients [2]. The combination of back pain and markers of inflammation (particularly erythrocyte sedimentation rate and C-reactive protein) should raise the suspicion for SEA and prompt further investigation with imaging. Lumbar puncture is not needed for diagnosis and carries the risk of inoculating the subarachnoid space with the organism. MRI with gadolinium contrast is the imaging study of choice as it allows for better delineation of the abscess from contiguous structures, making it advantageous over CT myelography. Treatment of choice is surgical decompression by laminectomy, in conjunction with IV antibiotics. However, conservative management with drainage of the abscess and 6 weeks of IV antibiotics have been shown to have success in stable patients with small abscesses and without neurologic symptoms [1-3, 9]. A meta-analysis found that medical therapy alone has a pooled failure rate of approximately 30%, but remains an option for patients who are poor surgical candidates [3, 9, 10].

In conclusion, this is a rare case of primary SEA caused by Streptococcus mitis in an immunocompetent adult with incidentally diagnosed ABPA. The presence of concurrent ABPA appeared unrelated, as this is a complex allergic pulmonary hypersensitivity. We do acknowledge that due to the lack of performing blood cultures we were unable to detect or rule out bacteremia. Improvement of the patient’s condition upon follow-up suggests that, while uncommon, conservative treatment with radiologically-guided drainage and IV antibiotics may be an option in hemodynamically stable patients without neurological symptoms. We believe this report highlights the complexity and difficulty in diagnosis and treatment of such a case, especially in the context of a lack of risk factors as seen in this patient.

Acknowledgments

Special thanks to Dr. Paramjit Chowdhry and Dr. Jenna Harmon from the Department of Radiology, Advocate Illinois Masonic Medical Center.

Conflict of Interest

None.

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