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Histoplasmosis

Last Updated: October 1, 2018

Open Table of Contents: Histoplasmosis

Figure 1: Multiple lesions scattered throughout the parenchyma demonstrating T1 hypointensity (top row left) and T2/FLAIR hyperintensity (top row right, second row left) with a rim of edema and a thin rim of enhancement (second row right). As is typical in fungal infections, the periphery demonstrates restricted diffusion (third row left, third row right), but not the center of the necrosis. SWI (bottom row) also demonstrates mild dark susceptibility artifact in the periphery of these lesions likely representing a combination of heavy metal deposition and microhemorrhage.

Figure 1: Multiple lesions scattered throughout the parenchyma demonstrating T1 hypointensity (top row left) and T2/FLAIR hyperintensity (top row right, second row left) with a rim of edema and a thin rim of enhancement (second row right). As is typical in fungal infections, the periphery demonstrates restricted diffusion (third row left, third row right), but not the center of the necrosis. SWI (bottom row) also demonstrates mild dark susceptibility artifact in the periphery of these lesions likely representing a combination of heavy metal deposition and microhemorrhage.

Description

  • Caused by dimorphic fungus Histoplasma Capsulatum
  • Exists as a mold in the environment and yeast at body temperatures
  • Endemic to Midwest
  • Disseminated disease is uncommon and occurs primarily when there is immune suppression
    • Represents the first manifestation of AIDS in 50-75% of patients
    • 5-10% of patients with dissemination develop CNS involvement

Pathology

  • Grows as a mold in the soil and causes infection when microconidia or hyphal elements are inhaled and convert into yeasts in the lungs or when organisms in old foci reactivate during immunosuppression

Clinical Features

  • Symptoms
    • Usually very nonspecific
  • Age or Gender
    • No predilection
  • Median survival
    • Variable
  • Associations
    • If available, look at prior chest imaging for calcified pulmonary nodules or mediastinal lymph nodes.

Imaging

  • General
    • Meningitis, scattered parenchymal lesions, abscesses and rarely histoplasmomas
    • Histoplasmomas: expansile lesion in the thalamus, hypothalamus or chiasmatic region that is small, round and demonstrates peripheral enhancement
  • Modality specific
    • CT
      • Enhancing mass lesions, atrophy and hydrocephalus
    • MR
      • T1WI
        • Hypointense lesions with surrounding hypointense edema
      • T2WI
        • Hyperintense lesions with surrounding hyperintense edema
        • If an abscess, the rim may be hypointense
      • DWI
        • Variable but typically no restriction
      • Contrast
        • Diffuse leptomeningeal enhancement
        • Ring enhancement typical of an abscess
  • Imaging Recommendations
    • Standard protocol MR (including DWI) with intravenous contrast
  • Mimic
    • Much like the other fungal infections, can mimic any of the ring enhancing lesions and can present as a nonspecific meningitis. Clinical history with travel to endemic areas can help narrow your differential diagnosis.

Contributor: Sean Dodson, MD

DOI: https://doi.org/10.18791/nsatlas.v1.03.02.17

References

Desai SP, et al. Disseminated CNS Histoplasmosis. AJNR. 1991; 12:290-92.

Jain KK, et al. Imaging features of central nervous system fungal infections. Neurol India. 2007; 55:241-50.

Saccente M. Central Nervous System Histoplasmosis. Curr Treat Options Neurol. 2008; 10(3):161-7.

Starkey J, et al. MRI of CNS Fungal Infections: Review of Aspergillosis to Histoplasmosis and Everything in Between. Clin Neuroradiol. 2014; 24(3):217-30.

Tabbal SD, et al. Cerebral Histoplasmosis. N Engl J Med. 1999; 340:1176.

Wheat LJ, et al. Diagnosis and Management of Central Nervous System Histoplasmosis. Clin Infect Dis. 2005; 40(6):844-852.

Zalduondo FM, et al. Meningitis, Vasculitis, and Cerebritis Caused by CNS Histoplasmosis: Radiologic-Pathologic Correlation. AJR. 1996; 166:194-96.

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