The Clinical Picture

Ring-enhancing cerebral lesions

Author and Disclosure Information

 

References

A 39-year-old woman with a history of human immunodeficiency virus (HIV) and hepatitis B virus infection was brought to the emergency department for evaluation of seizures, which had started a few days earlier. She was born and raised in a state bordering the Ohio River, an area where Histoplasma capsulatum is endemic. She denied any recent travel.

Ring-enhancing cerebral lesions
Figure 1. (A) Axial contrast-enhanced T1-weighted magnetic resonance imaging showed ring-enhancing lesions (white arrows), while (B) axial T2-weighted images showed ring-enhancing lesions surrounding hyperintensity, consistent with vasogenic edema (white arrows).

Her vital signs and neurologic examination were normal. Computed tomography of the head showed two areas of increased attenuation anterior to the frontal horns. To better characterize those lesions, magnetic resonance imaging (MRI) with contrast was done, which showed about a dozen 1-cm ring-enhancing lesions in the right cerebellum and both cerebral hemispheres (Figure 1).

Results of a complete blood cell count, metabolic profile, and chest radiography were normal. Her CD4 count was 428/μL (reference range 533–1,674) and 20% (60%–89%); her HIV viral load was 326,000 copies/mL.

She was initially treated empirically with sulfadiazine, pyrimethamine, and leukovorin for possible toxoplasmosis, which is the most common cause of ring-enhancing brain lesions in HIV patients. In the meantime, cerebrospinal fluid, blood, and urine were sent for a detailed workup for fungi, including Histoplasma. Results of the Histoplasma antibody and antigen studies of the serum, urine, and cerebrospinal fluid were positive, while cerebrospinal fluid testing for Toxoplasma by polymerase chain reaction testing was negative. Empirical treatment for toxoplasmosis was stopped and amphotericin B was started to treat disseminated histoplasmosis.

Figure 2. Partially organizing central nervous system abscess showing necrosis with acute inflammatory cells (1), fibrosis with acute and chronic inflammatory cells (2), and the normal-appearing brain tissue (3) (hematoxylin and eosin, × 4).

During her hospital course, she underwent brain biopsy via right frontotemporal craniotomy with resection of right frontal lesions. Pathologic study showed partially organizing abscesses with central necrosis (Figure 2), microscopy with Grocott-Gomori methenamine silver stain was positive for budding yeast forms consistent with H capsulatum (Figure 3), and special stain for acid-fast bacilli was negative for mycobacteria. Cultures of the brain biopsy specimen, blood, and cerebrospinal fluid for fungi, acid-fast bacilli, and bacteria did not reveal any growth after 28 days.

Figure 3. Grocott-Gomori methenamine silver staining of a biopsy specimen of a right frontal brain lesion showed budding yeast forms, consistent with Histoplasma capsulatum (× 100).

The patient was discharged home with instructions to take amphotericin B for a total of 6 weeks and then itraconazole. About 1 year later, she remained free of symptoms, although repeat MRI did not show any significant change in the size or number of histoplasmomas.

She did not comply well with her HIV treatment, and her immune status did not improve, so we decided to continue her itraconazole treatment for more than 1 year.

Next Article:

Evidence helps, but some decisions remain within the art of medicine

Related Articles

  • IM Board Review

    A young woman with enlarged lymph nodes

    A previously healthy 25-year-old woman presents with a “lump in the neck.” How should she be assessed?