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Central nervous system infections due to dematiaceous fungi (cerebral phaeohyphomycosis)

Central nervous system infections due to dematiaceous fungi (cerebral phaeohyphomycosis)
Author:
Gary M Cox, MD
Section Editor:
Carol A Kauffman, MD
Deputy Editor:
Keri K Hall, MD, MS
Literature review current through: Jan 2024.
This topic last updated: Jan 31, 2024.

INTRODUCTION — Dematiaceous fungi have melanin-like pigments in the cell walls and can cause a variety of infections in humans known as phaeohyphomycosis (phaeo is Greek for "dark"). The most severe of the phaeohyphomycoses are infections of the central nervous system. The nomenclature of these infections is confusing, and there are scant data on appropriate management. The mycology, clinical features, and treatment of cerebral phaeohyphomycosis will be reviewed here.

MYCOLOGY — The common factor among the dematiaceous fungi is the presence of melanin pigments in the cell walls and spores. These pigments cause the hyphae to appear golden brown when examined under the microscope, and this can sometimes suggest the diagnosis when examining clinical histopathology specimens. The fungal nomenclature of the agents of cerebral phaeohyphomycosis has undergone much change, and this has resulted in confusion about the identities of the causative fungi. The most common causes of cerebral phaeohyphomycosis, for example, are Cladosporium trichoides [1,2], Xylohypha bantiana [3-7], Cladosporium bantianum [8], and Cladophialophora bantiana [9]. It is now generally accepted that all of these fungi should be collectively known as Cladophialophora bantiana [10]. One can assume that all of the previous reports on infections due to these seemingly different fungi were caused by the same species.

Other causative fungi include Wangiella dermatitidis (also known as Exophiala dermatitidis) [11,12], Dactylaria gallopava (also known as Ochroconis gallopava) [13,14], Fonsecaea pedrosoi [15], Bipolaris spicifera (also known as Drechslera spicifera) [16,17], Rhinocladiella mackenziei (also known as Ramichloridium mackenziei and Ramichloridium obovoideum) [18,19], and Aureobasidium species [20]. Specimens are frequently not cultured; thus, species identifications are often not made [21]. In these cases, the diagnosis of phaeohyphomycosis depends upon demonstration of pigmented fungal structures by histopathology.

The dematiaceous fungi are found throughout the world in soil and decaying vegetation but appear to be especially common in tropical and subtropical regions. Most patients infected with R. mackenziei have been from Middle Eastern countries, including Saudi Arabia, Syria, or Kuwait [18,19,22,23], but cases have also been reported from India [24], Afghanistan [25], and Pakistan [26].

D. gallopava can causes encephalitis in turkeys, chickens, and other birds, but exposure to birds has not been linked to human disease [27-29].

PATHOGENESIS — Most cerebral infections are thought to be due to extension from the adjacent paranasal sinuses. It is presumed that spores enter the sinuses after inhalation and then proliferate, especially when the sinuses are obstructed. Some infections appear to have resulted directly from penetrating trauma to the head or from contaminated wounds [16]. Hematogenous dissemination to the central nervous system (CNS) has been postulated in some case reports, including a patient with localized skin lesions [20], a patient who injected drugs [9], and a heart-lung transplant patient with pneumonitis [30].

EPIDEMIOLOGY — Phaeohyphomycosis can occur in both immunocompetent and immunocompromised individuals. Approximately one half of the patients described in a review of 101 cases of CNS phaeohyphomycosis had no apparent immunocompromising condition [22]. Among immunocompromised patients, most cases have occurred in solid organ transplant recipients [1,13,22,30], patients with malignancies [14], and HIV-infected patients who injected illicit drugs [31].

Outbreaks related to contaminated glucocorticoids or other injectable solutions have also occurred, as discussed below. (See 'Outbreaks' below.)

CLINICAL FEATURES — Most cases of cerebral phaeohyphomycosis present as a brain abscess with focal neurologic deficits and/or generalized seizures. Fever and headache are uncommon. Symptomatic sinusitis or localized infection due to dematiaceous fungi at another site is very rare. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess".)

Neuroimaging studies usually show a single enhancing hypodense lesion in the frontal or parietal lobe, although many patients, especially those with underlying immunocompromising conditions, present with multiple lesions [32]. Meningeal enhancement is unusual, and there have been no reports of adjacent bone involvement.

DIAGNOSIS — The diagnosis is usually made by microscopic examination of the aspirated abscess fluid and/or resected tissue; histopathologic findings may reveal branching, septate hyphae that usually appear brown on hematoxylin and eosin staining or on potassium hydroxide (KOH) preparations of the material. However, the hyphae sometimes do not have pigment; in these instances, special stains for melanin can be used, such as the Fontana-Masson stain. Silver stains will obscure the fungi so that the brown color cannot be seen. Fungi in this group grow relatively quickly from clinical specimens. Identification of the species is based mostly upon morphology of sporulating cultures and often requires the assistance of reference laboratories.

TREATMENT — The treatment of cerebral phaeohyphomycosis requires both resection of the abscess and antifungal therapy. Complete surgical evacuation is optimal and is associated with a higher rate of success when compared with computed tomographic–guided aspiration. However, surgical removal of the abscess alone without antifungal therapy will most likely result in failure [33]. Susceptibility testing of the dematiaceous fungi has not been standardized; various studies have shown that many of these organisms are susceptible to itraconazole, voriconazole, posaconazole, and amphotericin B; some are susceptible to flucytosine, echinocandins, and terbinafine [34-40]. (See "Pharmacology of azoles" and "Pharmacology of amphotericin B".)

Reasonable recommendations for therapy, based upon the outcomes of published cases, should include surgical resection of the abscess and the administration of both amphotericin B and an azole (voriconazole [loading dose of 6 mg/kg intravenously [IV] every 12 hours for two doses followed by 4 mg/kg IV twice daily], or itraconazole [200 mg orally three times daily for three days, then 200 mg orally twice daily], or posaconazole delayed-release tablets [300 mg every 12 hours on the first day, then 300 mg once daily] [41]). We prefer liposomal amphotericin B (AmBisome, 3 to 5 mg/kg IV once daily) to amphotericin B deoxycholate (0.7 mg/kg IV once daily) given that the former agent is associated with less nephrotoxicity and infusion-related reactions and has improved CNS penetration in animal models. Among the azoles listed above, we prefer voriconazole because it has the best CNS penetration and is available as an IV formulation, which allows clinicians to rapidly and reliably achieve therapeutic drug levels when initiating therapy.

Voriconazole can be switched to the oral formulation at 200 mg twice daily if the patient is stable and is expected to be able to absorb oral medications. Amphotericin B can be stopped and therapy with the azole alone continued once the patient has had a clinical response and there has been documentation of therapeutic serum levels of the azole. (See "Pharmacology of azoles", section on 'Serum drug concentration monitoring'.)

Antifungal therapy should continue for at least six months, and courses of up to two years have been used.

The experience with using terbinafine, flucytosine, and echinocandins for cerebral infections is based on a few individual case reports, thus, it is not possible to recommend the use of these agents.

Survival rates for cerebral phaeohyphomycosis have improved with the availability of itraconazole and voriconazole but still are only approximately 50 percent at two years [10,22,42].

OUTBREAKS

Outbreak of fungal meningitis and osteoarticular infections — A multistate outbreak of fungal CNS infections (image 1) and osteoarticular infections (image 2) was detected in the United States in late September 2012 when over 700 patients who had received epidural injections of methylprednisolone produced at a single compounding center (New England Compounding Center) developed meningitis with or without posterior circulation stroke or paraspinal/spinal infections, and more than 30 patients who received osteoarticular injections of the same drug developed osteoarticular infections [43-49].

Of 753 cases reported from 20 states, there were 64 fatal cases; the following types of infections were reported [50]:

Meningitis only – 234 patients

Meningitis and paraspinal or spinal infection – 152 patients

Stroke (without lumbar puncture only) – 7 patients

Paraspinal or spinal infection only – 325 patients

Peripheral osteoarticular infection only – 33 patients

Paraspinal or spinal infection and peripheral joint infection – 2 patients

During the early investigation, the most common pathogen isolated from patients affected by the outbreak was Exserohilum spp, a dematiaceous fungus (picture 1) [47,51,52]. Other pathogens were detected (eg, Aspergillus fumigatus, Cladosporium spp) in a few patients [44,53].

A disproportionate number of patients in Michigan developed paraspinal or spinal infections as compared with meningitis [50,54], but the reasons for this remain unclear. Possible explanations include varying concentrations of fungus in specific drug lots and different injection techniques; the latter possibility remains speculative.

For patients who received an epidural injection with potentially contaminated methylprednisolone and who had any symptoms of CNS infection (eg, fever, new or worsening headache, photophobia, neck stiffness, nausea, or altered mental status) or stroke (weakness, slurred speech, confusion), a diagnostic lumbar puncture (LP) was recommended to be performed immediately, if not contraindicated [55]. Among 66 patients who met the case definition in a cohort analysis, an organism was identified in 22 patients (33 percent) [56]. Aspergillus fumigatus was cultured from the cerebrospinal fluid (CSF) of the index patient, but, in the remaining 21 patients, Exserohilum rostratum was identified from cultures of the CSF, tissue, or abscess fluid or was detected using polymerase chain reaction (PCR) in CSF or in tissue.

In these cases, as the sensitivity of CSF culture was fairly low, other methods were used to help establish the diagnosis including PCR and beta-D-glucan testing of CSF samples. 1,3-beta-D-glucan, a cell wall component of many fungi, is detected by the beta-D-glucan assay [57-59]. The beta-D-glucan assay may be positive in patients with a variety of invasive fungal infections. By studying 41 CSF specimens from confirmed cases of fungal meningitis and 66 negative control CSF specimens and by using a cut-off value of 138 pg/mL, the beta-D-glucan assay had a sensitivity of 100 percent and a specificity of 98 percent for the diagnosis of fungal meningitis associated with this outbreak [58]. Among 20 patients with serially collected samples (over months), most patients with a decline in beta-D-glucan concentrations had clinical improvement, but all four patients with continually elevated beta-D-glucan concentrations >500 pg/mL or concentrations that initially declined but later increased to >500 pg/mL had poor clinical outcomes, including stroke, relapse of meningitis, or soft tissue phlegmon.

In another study, in patients with CNS disease who did not have evidence of fungal CNS infection, beta-D-glucan concentrations were twofold lower in CSF than in serum, but in those with CNS fungal infections (including a variety of fungal infections, such as Exserohilum infection, candidiasis, coccidioidomycosis, and histoplasmosis), beta-D glucan concentrations were 25-fold higher in CSF than in serum [60].

The beta-D-glucan assay has not been cleared by the US Food and Drug Administration for use on CSF samples, and the cut-off value for this assay using CSF specimens has not been established. (See "Diagnosis of invasive aspergillosis", section on 'Beta-D-glucan assay' and "Clinical manifestations and diagnosis of candidemia and invasive candidiasis in adults", section on 'Beta-D-glucan assay'.)

For patients with fungal meningitis and spinal/paraspinal infection associated with contaminated methylprednisolone epidural injection, the United States Centers for Disease Control and Prevention (CDC) recommended antifungal therapy with voriconazole with or without liposomal amphotericin B (AmBisome) [61]. Liposomal amphotericin B therapy was stopped in many patients because of the expected side effects of infusion reactions, nephrotoxicity, and electrolyte loss. Patients taking voriconazole for infections caused by this outbreak complained of a "foggy" feeling, difficulty making decisions, forgetfulness, fatigue, nausea, anorexia, chapped lips, and alopecia and nail changes [62] in addition to the expected rash, photosensitivity, hallucinations, visual toxicities, and liver function test abnormalities.

Patients affected by the outbreak had a great deal of morbidity related to the infection itself and to the toxicity of the antifungal agents that were required to treat this infection [63]. Mortality rates were highest in those who had suffered a stroke with or without meningitis (>60 percent). Patients with isolated meningitis responded well to therapy and most were cured within six months. Many patients who had epidural abscesses/phlegmon and/or arachnoiditis required surgical intervention and prolonged antifungal therapy and were left with continuing problems of pain; some of these patients never returned to their preinfection functional status.

Other fungal outbreaks associated with contaminated solutions — In 2002, an outbreak of Exophiala (Wangiella) dermatitidis, another dematiaceous fungus, infections associated with epidural and intraarticular injections of contaminated methylprednisolone prepared at a compounding pharmacy affected five people (four with meningitis, one with sacroiliitis); two cases were fatal [64-66]. An investigation revealed several instances of nonadherence to sterile technique, including improper performance of an autoclave.

In 2016, an outbreak of E. dermatitidis and Rhodotorula mucilaginosa bloodstream infections associated with an intravenous (IV) flush solution compounded and administered at an oncology clinic in New York City occurred; 17 of 29 patients (59 percent) who received an IV medication at the clinic between January and May 2016 and who were available for evaluation were affected [67]. An investigation revealed that IV flush bags containing saline, heparin, vancomycin, and ceftazidime had been compounded under substandard conditions, stored in a refrigerator, and accessed daily for multiple patients over a one- to two-month period.

Information about other health care-associated outbreaks can be found on the CDC website.

SUMMARY AND RECOMMENDATIONS

Introduction − Dematiaceous fungi have melanin-like pigments in the cell walls and can cause a variety of infections in humans known as phaeohyphomycosis (phaeo is Greek for "dark"). The most severe of the phaeohyphomycoses are infections of the central nervous system (CNS). (See 'Introduction' above.)

Mycology

The fungal nomenclature of the agents of cerebral phaeohyphomycosis has undergone much change, and this has resulted in confusion about the identities of the causative fungi. The most common causes of cerebral phaeohyphomycosis, for example, are Cladophialophora bantiana, Wangiella dermatitidis, and Rhinocladiella mackenziei. (See 'Mycology' above.)

The dematiaceous fungi are found throughout the world in soil and decaying vegetation but appear to be especially common in tropical and subtropical regions. (See 'Mycology' above.)

Pathogenesis − Most cerebral infections are thought to be due to extension from the adjacent paranasal sinuses. It is presumed that spores enter the sinuses after inhalation and then proliferate, especially when the sinuses are obstructed. (See 'Pathogenesis' above.)

Epidemiology − Approximately one half of the patients with CNS phaeohyphomycosis have no apparent immunocompromising condition. Among immunocompromised patients, most cases have occurred in solid organ transplant recipients, patients with malignancies, and HIV-infected patients who injected illicit drugs. Outbreaks related to contaminated glucocorticoids (including a large outbreak in the United States in 2012) or other injectable solutions have also occurred. (See 'Epidemiology' above and 'Outbreaks' above.)

Clinical features − Most cases of cerebral phaeohyphomycosis present as a brain abscess with focal neurologic deficits and/or generalized seizures. Fever and headache are uncommon. (See 'Clinical features' above.)

Diagnosis − The diagnosis is usually made by microscopic examination of the aspirated abscess fluid and/or resected tissue; histopathologic findings may reveal branching, septate hyphae that usually appear brown on hematoxylin and eosin staining or on potassium hydroxide (KOH) preparations of the material. Identification of the species is based mostly upon morphology of sporulating cultures and often requires the assistance of reference laboratories. (See 'Diagnosis' above.)

Treatment

The treatment of cerebral phaeohyphomycosis requires both resection of the abscess and antifungal therapy. Complete surgical evacuation is optimal and is associated with a higher rate of success when compared with computed tomographic–guided aspiration. (See 'Treatment' above.)

Reasonable recommendations for therapy based upon the outcomes of published cases starts with surgical resection of the abscess and the administration of both amphotericin B and an azole (voriconazole, itraconazole, or posaconazole). We prefer liposomal amphotericin B (AmBisome) to amphotericin B deoxycholate given that the former agent is associated with less nephrotoxicity and infusion-related reactions and has improved CNS penetration in animal models. Among the azoles listed above, we prefer voriconazole because it has the best CNS penetration and is available in an IV formulation. (See 'Treatment' above.)

Antifungal therapy should continue for at least six months, and courses of up to two years have been used. (See 'Treatment' above.)

Prognosis − The mortality rate among patients with these infections is at least 50 percent; the high mortality rate highlights the need for aggressive therapy. (See 'Treatment' above.)

  1. Aldape KD, Fox HS, Roberts JP, et al. Cladosporium trichoides cerebral phaeohyphomycosis in a liver transplant recipient. Report of a case. Am J Clin Pathol 1991; 95:499.
  2. Banerjee U, Mohapatra AK, Sarkar C, Chaudhery R. Cladosporiosis (cerebral phaeohyphomycosis) of brain--a case report. Mycopathologia 1989; 105:163.
  3. Buxi TB, Prakash K, Vohra R, Bhatia D. Imaging in phaeohyphomycosis of the brain: case report. Neuroradiology 1996; 38:139.
  4. Lirng JF, Tien RD, Osumi AK, et al. Cerebral phaeohyphomycosis complicated with brain abscess: a case report. Zhonghua Yi Xue Za Zhi (Taipei) 1995; 55:491.
  5. Mukherji SK, Castillo M. Cerebral phaeohyphomycosis caused by Xylohypha bantiana: MR findings. AJR Am J Roentgenol 1995; 164:1304.
  6. Palaoglu S, Sav A, Basak T, et al. Cerebral phaeohyphomycosis. Neurosurgery 1993; 33:894.
  7. Sekhon AS, Galbraith J, Mielke BW, et al. Cerebral phaeohyphomycosis caused by Xylohypha bantiana, with a review of the literature. Eur J Epidemiol 1992; 8:387.
  8. Hironaga M, Watanabe S. Cerebral phaeohyphomycosis caused by Cladosporium bantianum: a case in a female who had cutaneous alternariosis in her childhood. Sabouraudia 1980; 18:229.
  9. Walz R, Bianchin M, Chaves ML, et al. Cerebral phaeohyphomycosis caused by Cladophialophora bantiana in a Brazilian drug abuser. J Med Vet Mycol 1997; 35:427.
  10. Kantarcioglu AS, Guarro J, De Hoog S, et al. An updated comprehensive systematic review of Cladophialophora bantiana and analysis of epidemiology, clinical characteristics, and outcome of cerebral cases. Med Mycol 2017; 55:579.
  11. Chang CL, Kim DS, Park DJ, et al. Acute cerebral phaeohyphomycosis due to Wangiella dermatitidis accompanied by cerebrospinal fluid eosinophilia. J Clin Microbiol 2000; 38:1965.
  12. Tintelnot K, de Hoog GS, Thomas E, et al. Cerebral phaeohyphomycosis caused by an Exophiala species. Mycoses 1991; 34:239.
  13. Vukmir RB, Kusne S, Linden P, et al. Successful therapy for cerebral phaeohyphomycosis due to Dactylaria gallopava in a liver transplant recipient. Clin Infect Dis 1994; 19:714.
  14. Sides EH 3rd, Benson JD, Padhye AA. Phaeohyphomycotic brain abscess due to Ochroconis gallopavum in a patient with malignant lymphoma of a large cell type. J Med Vet Mycol 1991; 29:317.
  15. al-Hedaithy SS, Jamjoom ZA, Saeed ES. Cerebral phaeohyphomycosis caused by Fonsecaea pedrosoi in Saudi Arabia. APMIS Suppl 1988; 3:94.
  16. Biggs PJ, Allen RL, Powers JM, Holley HP Jr. Phaeohyphomycosis complicating compound skull fracture. Surg Neurol 1986; 25:393.
  17. Yoshimori RN, Moore RA, Itabashi HH, Fujikawa DG. Phaeohyphomycosis of brain: granulomatous encephalitis caused by Drechslera spicifera. Am J Clin Pathol 1982; 77:363.
  18. Podnos YD, Anastasio P, De La Maza L, Kim RB. Cerebral phaeohyphomycosis caused by Ramichloridium obovoideum (Ramichloridium mackenziei): case report. Neurosurgery 1999; 45:372.
  19. Sutton DA, Slifkin M, Yakulis R, Rinaldi MG. U.S. case report of cerebral phaeohyphomycosis caused by Ramichloridium obovoideum (R. mackenziei): criteria for identification, therapy, and review of other known dematiaceous neurotropic taxa. J Clin Microbiol 1998; 36:708.
  20. Fletcher H, Williams NP, Nicholson A, et al. Systemic phaeohyphomycosis in pregnancy and the puerperium. West Indian Med J 2000; 49:79.
  21. Masini T, Riviera L, Cappricci E, Arienta C. Cerebral phaeohyphomycosis. Clin Neuropathol 1985; 4:246.
  22. Revankar SG, Sutton DA, Rinaldi MG. Primary central nervous system phaeohyphomycosis: a review of 101 cases. Clin Infect Dis 2004; 38:206.
  23. Kantarcioglu AS, de Hoog GS. Infections of the central nervous system by melanized fungi: a review of cases presented between 1999 and 2004. Mycoses 2004; 47:4.
  24. Badali H, Chander J, Bansal S, et al. First autochthonous case of Rhinocladiella mackenziei cerebral abscess outside the Middle East. J Clin Microbiol 2010; 48:646.
  25. Cristini A, Garcia-Hermoso D, Celard M, et al. Cerebral phaeohyphomycosis caused by Rhinocladiella mackenziei in a woman native to Afghanistan. J Clin Microbiol 2010; 48:3451.
  26. Jabeen K, Farooqi J, Zafar A, et al. Rhinocladiella mackenziei as an emerging cause of cerebral phaeohyphomycosis in Pakistan: a case series. Clin Infect Dis 2011; 52:213.
  27. Salkin IF, Dixon DM, Kemna ME, et al. Fatal encephalitis caused by Dactylaria constricta var. gallopava in a snowy owl chick (Nyctea scandiaca). J Clin Microbiol 1990; 28:2845.
  28. Blalock HG, Georg LK, Derieux WT. Encephalitis in turkey poults due to Dactylaria (Diplorhinotrichum) gallopava--a case report and its experimental reproduction. Avian Dis 1973; 17:197.
  29. Ranck FM Jr, Georg LK, Wallace DH. Dactylariosis--a newly recognized fungus disease of chickens. Avian Dis 1974; 18:4.
  30. Levin TP, Baty DE, Fekete T, et al. Cladophialophora bantiana brain abscess in a solid-organ transplant recipient: case report and review of the literature. J Clin Microbiol 2004; 42:4374.
  31. del Palacio-Hernanz A, Moore MK, Campbell CK, et al. Infection of the central nervous system by Rhinocladiella atrovirens in a patient with acquired immunodeficiency syndrome. J Med Vet Mycol 1989; 27:127.
  32. Roche M, Redmond RM, O'Neill S, Smyth E. A case of multiple cerebral abscesses due to infection with Cladophialophora bantiana. J Infect 2005; 51:e285.
  33. Delfino D, De Hoog S, Polonelli L, et al. Survival of a neglected case of brain abscess caused by Cladophialophora bantiana. Med Mycol 2006; 44:651.
  34. Al-Abdely HM, Najvar L, Bocanegra R, et al. SCH 56592, amphotericin B, or itraconazole therapy of experimental murine cerebral phaeohyphomycosis due to Ramichloridium obovoideum ("Ramichloridium mackenziei"). Antimicrob Agents Chemother 2000; 44:1159.
  35. Caligiorne RB, Resende MA, Melillo PH, et al. In vitro susceptibility of chromoblastomycosis and phaeohyphomycosis agents to antifungal drugs. Med Mycol 1999; 37:405.
  36. Espinel-Ingroff A, Boyle K, Sheehan DJ. In vitro antifungal activities of voriconazole and reference agents as determined by NCCLS methods: review of the literature. Mycopathologia 2001; 150:101.
  37. Fothergill AW, Rinaldi MG, Sutton DA. Antifungal susceptibility testing of Exophiala spp.: a head-to-head comparison of amphotericin B, itraconazole, posaconazole and voriconazole. Med Mycol 2009; 47:41.
  38. Rivard RG, McCall S, Griffith ME, et al. Efficacy of caspofungin and posaconazole in a murine model of disseminated Exophiala infection. Med Mycol 2007; 45:685.
  39. Espinel-Ingroff A. In vitro antifungal activities of anidulafungin and micafungin, licensed agents and the investigational triazole posaconazole as determined by NCCLS methods for 12,052 fungal isolates: review of the literature. Rev Iberoam Micol 2003; 20:121.
  40. Deng S, Pan W, Liao W, et al. Combination of Amphotericin B and Flucytosine against Neurotropic Species of Melanized Fungi Causing Primary Cerebral Phaeohyphomycosis. Antimicrob Agents Chemother 2016; 60:2346.
  41. Proia LA, Trenholme GM. Chronic refractory phaeohyphomycosis: successful treatment with posaconazole. Mycoses 2006; 49:519.
  42. Matsumoto T, Matsuda T, McGinnis MR, Ajello L. Clinical and mycological spectra of Wangiella dermatitidis infections. Mycoses 1993; 36:145.
  43. Centers for Disease Control and Prevention. Multi-state meningitis outbreak. http://www.cdc.gov/hai/outbreaks/meningitis.html (Accessed on January 15, 2013).
  44. Centers for Disease Control and Prevention (CDC). Multistate outbreak of fungal infection associated with injection of methylprednisolone acetate solution from a single compounding pharmacy - United States, 2012. MMWR Morb Mortal Wkly Rep 2012; 61:839.
  45. Lyons JL, Gireesh ED, Trivedi JB, et al. Fatal exserohilum meningitis and central nervous system vasculitis after cervical epidural methylprednisolone injection. Ann Intern Med 2012; 157:835.
  46. Pettit AC, Kropski JA, Castilho JL, et al. The index case for the fungal meningitis outbreak in the United States. N Engl J Med 2012; 367:2119.
  47. Smith RM, Schaefer MK, Kainer MA, et al. Fungal infections associated with contaminated methylprednisolone injections. N Engl J Med 2013; 369:1598.
  48. Bell BP, Khabbaz RF. Responding to the outbreak of invasive fungal infections: the value of public health to Americans. JAMA 2013; 309:883.
  49. Pettit AC, Malani AN. Outbreak of fungal infections associated with contaminated methylprednisolone acetate: an update. Curr Infect Dis Rep 2015; 17:441.
  50. Centers for Disease Control and Prevention. Multistate fungal meningitis outbreak - current case count. http://www.cdc.gov/hai/outbreaks/meningitis-map-large.html (Accessed on November 11, 2015).
  51. Lockhart SR, Pham CD, Gade L, et al. Preliminary laboratory report of fungal infections associated with contaminated methylprednisolone injections. J Clin Microbiol 2013; 51:2654.
  52. Chiller TM, Roy M, Nguyen D, et al. Clinical findings for fungal infections caused by methylprednisolone injections. N Engl J Med 2013; 369:1610.
  53. Center for Infectious Disease Research & Policy. Warnings, cases expand in fungal meningitis outbreak. http://www.cidrap.umn.edu/cidrap/content/other/news/oct1612fungusbr.html (Accessed on October 17, 2012).
  54. Kuehn BM. Hospital faces uncertainty as it copes with surge of patients with fungal meningitis. JAMA 2013; 309:219.
  55. Centers for Disease Control and Prevention. Multistate fungal meningitis outbreak investigation. What should physicians be doing? http://www.cdc.gov/hai/outbreaks/clinicians/what-physicians-should-be-doing.html (Accessed on October 14, 2012).
  56. Kainer MA, Reagan DR, Nguyen DB, et al. Fungal infections associated with contaminated methylprednisolone in Tennessee. N Engl J Med 2012; 367:2194.
  57. Lyons JL, Roos KL, Marr KA, et al. Cerebrospinal fluid (1,3)-β-D-glucan detection as an aid for diagnosis of iatrogenic fungal meningitis. J Clin Microbiol 2013; 51:1285.
  58. Litvintseva AP, Lindsley MD, Gade L, et al. Utility of (1-3)-β-D-glucan testing for diagnostics and monitoring response to treatment during the multistate outbreak of fungal meningitis and other infections. Clin Infect Dis 2014; 58:622.
  59. Malani AN, Singal B, Wheat LJ, et al. (1,3)-β-d-glucan in cerebrospinal fluid for diagnosis of fungal meningitis associated with contaminated methylprednisolone injections. J Clin Microbiol 2015; 53:799.
  60. Lyons JL, Thakur KT, Lee R, et al. Utility of measuring (1,3)-β-d-glucan in cerebrospinal fluid for diagnosis of fungal central nervous system infection. J Clin Microbiol 2015; 53:319.
  61. Centers for Disease Control and Prevention. Interim treatment guidance for central nervous system and parameningeal infections associated with injection of contaminated steroid products. http://www.cdc.gov/hai/outbreaks/clinicians/guidance_cns.html (Accessed on March 06, 2013).
  62. Malani AN, Kerr L, Obear J, et al. Alopecia and nail changes associated with voriconazole therapy. Clin Infect Dis 2014; 59:e61.
  63. Malani AN, Kauffman CA, Latham R, et al. Long-term Outcomes of Patients With Fungal Infections Associated With Contaminated Methylprednisolone Injections. Open Forum Infect Dis 2020; 7:ofaa164.
  64. Centers for Disease Control and Prevention (CDC). Exophiala infection from contaminated injectable steroids prepared by a compounding pharmacy--United States, July-November 2002. MMWR Morb Mortal Wkly Rep 2002; 51:1109.
  65. Perfect JR. Iatrogenic fungal meningitis: tragedy repeated. Ann Intern Med 2012; 157:825.
  66. Macher AM. Iatrogenic fungal meningitis. Ann Intern Med 2013; 158:364.
  67. Vasquez AM, Lake J, Ngai S, et al. Notes from the Field: Fungal Bloodstream Infections Associated with a Compounded Intravenous Medication at an Outpatient Oncology Clinic - New York City, 2016. MMWR Morb Mortal Wkly Rep 2016; 65:1274.
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References

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