Intracranial Nocardia in the setting of AIDS

Abstract

Nocardia intracranial abscesses occur almost exclusively in patients who are immunocompromised due to diabetes, transplantation, or HIV/AIDS. Patients usually present with seizures, headaches, fevers, and menin-gismus. Laboratory evaluation is nonspecific but may reveal an elevated erythrocyte sedimentation rate and white blood cell count. An important task in the workup of intracranial infection is searching for local causes such as sinusitis, otitis media, or mastoiditis.

CASE PRESENTATION

A 44-year-old man with HIV and a CD4 count of 15 was admitted for Candida esophagitis as well as pneumonia. He presented to the emergency department following a fall. For the week prior to admission, he had trouble concentrating, developed memory loss, and became weak. This was associated with mild headaches and subjective fevers. During a prior admission, he underwent bronchoscopy before discharge, which was unremarkable, but the bronchoalveolar lavage grew Nocardia after discharge. Prior to presentation to our emergency department, the patient had been placed on Bactrim. However, it is unclear whether the patient was compliant with this therapy. At the time of presentation, the initial physical examination findings revealed word-finding difficulties consistent with Broca's aphasia. He had trouble with fine and coarse motor activity. He also had severe thrush of the oral mucosa.

Initial computed tomography (CT) brain examination demonstrated vague heterogenous mixed hyperdensities in the gray-white junctions of the frontoparietal lobes bilaterally as well as extensive surrounding hypoattenuation in the subcortical white matter. Following contrast infusion, this area corresponded to a ring-enhancing cluster of lesions centered within the bilateral frontoparietal junction. These findings can present a broad differential diagnosis, ranging from infectious and inflammatory etiologies as well as neoplastic etiologies—both primary central nervous system malignancies and lymphoma as well as metastatic disease—and vascular abnormalities such as aneurysms or arteriovenous malformations. These findings were also seen in conjunction with a cavitary necrotic mass in the superior segment of the right lower lobe (Figure 1).

Figure 1.

Noncontrast CT of the chest reveals a cavitary mass (arrow) within the apical segment right lower lobe.

Subsequent magnetic resonance imaging (MRI) demonstrated restricted diffusion in the region of heterogeneous attenuation on CT at the gray-white junction of the bilateral frontoparietal lobes (Figures 2b and 2d). These lesions also showed rim enhancement on the postgadolinium T1-weighted images (Figures 2a and 2c). The expected diffuse T2 and fluid-attenuated inversion recovery hyperintense signal consistent with edema was seen in the subcortical white matter and extended to cortices in these regions. A slight hypointense rim was also evident, which represented the fibrous capsule that enhances on postgadolinium T1 images (Figure 2a and 2c).

Figure 2.

(a, c) Postinfusion MRI of the brain showing ring-enhancing clusters of lesions within the bilateral parietal lobes associated with vasogenic edema. (b, d) Corresponding diffusion images show that these lesions are diffusion restricted.

Following the MRI findings and history of Nocardia pneumonia, the patient underwent treatment with high-dose Bactrim, high-dose meropenem, and amikacin. The diagnosis of intracranial Nocardia was confirmed following brain biopsy, which revealed gram-positive filamentous branching rods, which later turned out to be Nocardia. The patient was discharged to a long-term acute care center for long-term antibiotic therapy. Eventually the patient underwent operative drainage of the intracranial abscesses and improved clinically.

DISCUSSION

Imaging evaluation of the intracranial contents often starts with a noninfusion CT examination followed by further characterization by intracranial MRI with and without contrast. Infectious and inflammatory pathologies classically have nonspecific findings on unenhanced CT and have much more characteristic findings on contrast-enhanced MRI.

Differential considerations for multiple rim-enhancing intracranial masses in the setting of HIV/AIDS or an immunocompromised state include toxoplasmosis, tuberculosis, pyogenic/fungal abscess, and lymphoma. Toxoplasmosis is the most common opportunistic infection and usually involves the basal ganglia or gray-white junction commonly associated with surrounding edema. The abscess cavity contains an eccentric enhancing nodule. Lymphoma presents as either peripherally enhancing/centrally necrotic or homogeneously enhancing lesions. Abscess presents as diffusion-restricted ring-enhancing lesions. Tuberculosis typically presents as a solid or rim-enhancing lesion. As in our case, diffusion restriction favors diagnosis of intracranial abscess.

Treatment of intracranial Nocardia abscess includes intravenous therapy with two antibiotics, such as trimethoprim/sulfamethoxazole plus amikacin. Eventually the patient can be transitioned to oral agents. These include a sulfonamide, minocycline, and/or amoxicillin clavulanate (1). Generally, the clinical outcome is good when the diagnosis is not significantly delayed and the duration of therapy is appropriate. In one study, no relapse of disease was seen in HIV patients when treated for a mean period of 45 weeks (2).