Invasive fungal sinusitis caused by Pseudallescheria boydii: case report and literature review.
Fungal sinusitis secondary to Pseudallescheria boydii is rare, as only 25 cases have been previously reported in the literature. Although P boydii resembles Aspergillus on pathologic examination, it is typically resistant to amphotericin B. Therefore, culture is necessary to differentiate the two. Patients with P boydii sinusitis should generally be treated with a combination of surgery and antifungal therapy. Combination treatment is particularly important for immunocompromised patients with fungal invasion because mortality among these patients is high. The prognosis is better for immunocompetent patients, even those with fungal invasion. We describe a new case of invasive fungal sinusitis secondary to P boydii infection, and we review the literature on this emerging pathogen.
Pseudallescheria boydii--a ubiquitous, saprophytic fungus in the class Ascomycetes--is an emerging pathogen found worldwide. It is commonly isolated in soil, in polluted and coastal waters, and in animal manure. (1) Siebenmann first isolated the organism in the 1880s as a pathogen in the ear of a child with chronic otitis externa. (2) The first complete description of the organism was published in 1922 by Shear. (3)
P boydii is associated with Madura foot (maduromycosis), a cutaneous and subcutaneous suppurative disease that affects farmers in tropical and subtropical countries. (4) Historically, Madura foot has accounted for 99% of all P boydii infections. (1) The organism has also been identified in specimens obtained from pulmonary cavities and pulmonary infiltrates. It has been shown to cause sinusitis, corneal infections, endophthalmitis, parotitis, skin infections, arthritis, osteomyelitis, brain and thyroid abscesses, endocarditis, chronic prostatitis, and disseminated infection?
In this article, we describe a case of P boydii invasive fungal sinusitis in a diabetic patient who died before the pathogen was identified. As we discuss, this organism can be mistaken for Aspergillus on fungal smear, but it is typically resistant to amphotericin B, the antifungal medication that is commonly started empirically for patients with invasive fungal sinusitis. Thus, in cases of invasive fungal sinusitis, proper identification via culture is imperative to ensure effective pharmacotherapy.
A 76-year-old man with non-insulin-dependent (type 2) diabetes mellitus presented with a 4-month history of intractable temporal and occipital headaches. Since the onset of the headaches, he had been diagnosed with sinusitis and treated twice with a penicillin derivative, but his headaches did not resolve. Two subsequent courses of a steroid taper provided no relief. At that point, the patient was admitted to our hospital for a further workup.
Upon admission, the patient was dehydrated and hyperglycemic; a finger-stick blood test revealed that his glucose level was 477 mg/dl. He had discontinued his oral hypoglycemic medication prior to admission, despite being on a steroid course. The early part of his hospitalization was complicated by the medical and later surgical treatment of diverticulitis. After one of his abdominal surgeries, he awoke from surgery confused and combative and complaining of blindness in both eyes. Prior to the onset of the blindness, the patient's visual acuity had been 20/60 in the right eye and 6/200 in the left eye; he had also had a left relative afferent pupillary defect. However, after the onset of the blindness, he was found to have a disconjugate gaze with poor extraocular motility (worse in the left eye), and he was not able to perceive hand movements in front of his eyes.
The laboratory workup revealed an elevated white blood cell (WBC) count of 12.6 x [10.sup.9]/L (normal: 4.8 to 10.8), an elevated erythrocyte sedimentation rate of 81 mm/hr (normal: 0 to 20), and an elevated glycosylated hemoglobin concentration of 11.2% (normal: 4.5 to 6.4%). The rapid plasma reagin test was nonreactive, and the vitamin [B.sub.12] level was elevated at 1,143 pg/ml (normal: 210 to 705). Alumbar puncture revealed a low cerebrospinal fluid (CSF) glucose concentration of 104 mg/dl (normal: 239 to 358 for a blood glucose level of 477 mg/dl) and an elevated CSF protein level of 49.2 mg/dl (normal: 15 to 45); no WBCs were found in the CSF.
Noncontrast computed tomography (CT) of the head showed at partial opacification at the sphenoid sinus. Contrast-enhanced magnetic resonance imaging (MRI) of the brain demonstrated enhancement of the dura along the planum sphenoidale, the anterior frontal lobes bilaterally, and the orbital apices bilaterally (figure 1). Enhancement was also noted along the anterior clinoid. Bilateral engorgement of the superior orbital veins was noted.
[FIGURE 1 OMITTED]
Nasal endoscopy detected no necrosis of any turbinate or of the rostra of the sphenoid sinuses (figure 2). Contrast-enhanced CT of the sinuses revealed mucoperiosteal thickening of the right sphenoid and frontal sinuses and opacification of the left sphenoid sinus (figure 3). Enhancing soft tissue was seen at the posterior wall of the frontal sinus, and it extended along the planum sphenoidale and through the fovea ethmoidalis; intracranial extension was seen along the dura at the anterior cranial fossa and the anterior aspect of the interhemispheric falx (figure 4). Additionally, the process extended anteriorly through the optic nerve foramina and superior orbital fissures and was associated with a loss of normal fat planes bilaterally in the pterygopalatine fossae. Bone erosion accompanied the abnormal soft-tissue extension from the ethmoid air cells and frontal sinuses through the adjacent anterior cranial floor and cribriform plate.
[FIGURES 2-4 OMITTED]
In light of these findings, the patient was placed on empiric piperacillin/tazobactam and amphotericin B lipid complex to cover bacterial skull base osteomyelitis and invasive fungal sinusitis. He was then taken to the operating room for image-guided bilateral endoscopic sphenoidotomy with biopsy. Operative findings included minimally inflamed mucosa within the nasal cavity. No necrotic tissue was present on the right or left sphenoid rostrum, and no purulent or necrotic debris was present in either sphenoid sinus (figure 5). A frozen-section biopsy of the right sphenoid sinus was reported as only inflamed mucosa with no evidence of invasive fungal disease. A Gram's stain of the sinus contents identified gram-positive cocci and yeast. Final pathology identified a mass of fungal hyphae in 1 of 5 specimens that were morphologically consistent with the presence of Aspergillus spp. Culture grew 2+ coagulase-negative staphylococci and 1+ multidrug-resistant Klebsiella pneumoniae. Based on these findings, the antibacterial coverage was changed to vancomycin and meropenem.
[FIGURE 5 OMITTED]
Over the next several days, the patient's mental status worsened. A cerebral angiogram showed an area of opacification within the anterior aspect of the left cavernous sinus consistent with thrombosis. Hence, the patient was started on heparin anticoagulation. However, his mental status continued to worsen, and he developed epistaxis that required packing of the left nasal cavity. The heparin drip was discontinued, but soon thereafter, he developed worsening respiratory distress and died. Of note, he had been switched from amphotericin B lipid complex to voriconazole approximately 3 days prior to his death because the maximum amphotericin B dosage had been reached.
At autopsy, the dura of the anterior falx cerebri was indurated and thickened (as much as 0.5 cm). Microscopic examination of this area detected acute and chronic inflammation associated with necrosis and a granulomatous component. Silver stains showed septate fungal hyphae. Fungal cultures from the sphenoid biopsies performed at surgery grew P boydii in the postmortem period.
For our literature review, we searched the PubMed database, using the keywords Pseudallescheria, boydii, Verticillium graphii, Allescheria, Glenospora, Indiella americanus, Acremoniella lusii, Petriellidium, Scedosporium apiospermum, monosporium, and sinusitis. We found 25 reported cases of sinusitis that were caused by P boydii. (5-29) The case described in this article brings to 26 the total number of cases documented in the literature (table). These patients included 17 women and 9 men, aged 20 to 85 years (mean: 48.3). The first case was reported by Gluckman et al in 1977; their patient was a 58-year-old diabetic man on hemodialysis who ultimately died of a cause unrelated to his P boydii infection. (6)
Of the 26 cases, mucosal invasion by fungal organisms was proven or suspected in 12 patients, excluded or not suspected in 9 patients, and unknown in the remaining 5 patients. Of the 12 patients with proven or suspected invasive disease, 9 were immunocompromised; 4 patients had leukemia, 3 were diabetics, and 2 had acquired immunodeficiency syndrome (AIDS). All 9 of these patients either died of infection or another cause or had persistent or recurrent infection at the time the case was reported. Six of these 9 immunocompromised patients were treated with surgery and antifungal therapy, 1 was treated with surgery and antibacterial therapy, and 2 were treated with antifungal therapy alone. Of the 3 immunocompetent patients with proven or suspected invasive disease, 1 experienced a complete resolution of disease after undergoing combined surgery and antifungal therapy, 1 responded completely to surgery alone, and 1 died of infection after being treated with combined surgery and antifungal therapy.
Five of the 9 patients without evidence or suspicion of invasion were immunocompetent, and all 5 experienced a complete resolution of their infection; 4 patients had been treated with surgery alone and the other with combined surgery and antifungal therapy. Of the 4 patients without signs of invasion who were immunocompromised (1 case each of adrenocortical insufficiency, sickle cell anemia, diabetes, and organ transplantation), 1 patient experienced a full resolution with combined surgery and antifungal therapy, 1 recovered completely with surgery alone, 1 died of squamous cell carcinoma of the sinuses following surgery, and the outcome of the other patient, who had undergone surgery, was not reported.
Among the 5 patients in whom the presence or absence of fungal invasion was not reported, 2 were immunosuppressed (1 case of diabetes and 1 case of bone marrow transplantation); the diabetic patient was treated with surgery alone and his outcome was not reported, and the post-transplant patient was treated with combined surgery and antifungal therapy but died of a related cause. Of the 3 immunocompetent patients in whom the presence or absence of fungal invasion was not reported, all experienced a complete resolution of symptoms; 2 had been treated with surgery alone, and 1 had been treated with combined surgery and antifungal therapy.
Among the 26 cases, the maxillary sinuses were involved in 15 cases, the sphenoid sinuses in 14, the ethmoid sinuses in 9, the frontal sinuses in 2, and the nasal cavity only in 1. Seven of the 14 patients with sphenoid sinus involvement had isolated sphenoid disease.
Of the 26 patients, 13 had concomitant bacterial infections; these pathogens included K pneumoniae (n = 3), Staphylococcus aureus (3), Citrobacter freundii (3), Staphylococcus epidermidis (3), Proteus mirabilis (2), Enterobacter cloacae (2), anaerobic gram-positive rods (1), Serratia liquefasciens (1), and Klebsiella oxytoca (1). Fungal coinfection (Candida albicans) was seen in 1 patient.
Fungal infection of the paranasal sinuses includes a broad spectrum of disease processes. At one end of the spectrum is allergic fungal sinusitis, which represents an immune reaction to noninvading fungal colonizers that was first associated with Aspergillus. (30) At the other end of the spectrum is acute invasive fungal sinusitis, which is usually caused by Mucor or Aspergillus spp. Intermediate disease processes include chronic invasive fungal sinusitis and chronic noninvasive fungal sinusitis (fungus ball). In 1997, deShazo et al proposed that invasive fungal sinusitis be classified into three categories: granulomatous, acute fulminant, and chronic. (31) They described 2 cases of chronic invasive sinusitis in middle-aged adults with well-controlled non-insulin-dependent diabetes mellitus and apical orbital syndrome. The 2 patients had a similar course: protracted disease for more than 6 months with proptosis, vision changes, and late neurologic symptoms reflecting cavernous sinus invasion. Both patients died of their infection. Our patient followed a similar course with several months of protracted headache.
Aspeligillus, Mucor, and Candida spp. are responsible for most pathologic fungal sinus infections. (32) However, improvements in the medical management of immunosuppressed patients and the wider use of immunosuppressive therapies has led to the identification of a long list of unusual fungal pathogens, some of which were previously thought to be solely commensal. Specifically, rare fungal pathogens have been isolated in AIDS patients, (22) in cancer patients (particularly those being treated for leukemia (33)), and in transplant recipients. (34) One of these emerging pathogens is P boydii.
P boydii has undergone many name changes over the years. In his original report, Siebenmann called it Verticillium graphii. (2) It has since been referred to as Allescheria boydii, Glenospora boydii, Indiella americanus, and Acremoniella lusii. (14) In 1970, Malloch suggested that the species be transferred from the genus Allescheria to Petriellidium. (35) This change was later thought to be an error, and the organism was placed in the valid and previously described genus Pseudallescheria. (1) The anamorph (imperfect) form of the organism is called Scedosporium apiospermum (formerly Monosporium apiospermum), and was shown by Emmons (36) in 1944 to be the same organism as P boydii. Both forms have been implicated as pathogens.
Of the 26 cases (5-29) of fungal sinusitis secondary to P boydii infection that have now been reported in the literature, fungal invasion was proven or suspected in 12 patients, 9 of whom were immunocompromised. It is interesting that the other 3 patients with invasive disease were immunocompetent: 2 experienced a full resolution of infection (1 with combination surgery and antifungal therapy and the other with surgery alone). Among the 13 patients with immunosuppression whose outcome was reported, I 1 either died or had persistent or recurrent infection by the time the case was reported. Two patients with immunosuppression experienced a complete resolution of the infection, but neither had evidence of invasion: 1 of these patients had been treated with combined surgery and antifungal therapy and the other had been treated with surgery alone. These data suggest that our patient's prognosis probably would have been poor even if he had been diagnosed sooner.
Identification of P boydii by fungal culture is essential to selecting effective pharmacotherapy. The hyphae of P boydii can resemble those of Aspergillus on fungal stains, and their tropism for blood vessels is similar. (15) But unlike Aspergillus, P boydii is typically resistant to amphotericin B. (37) This can be problematic because amphotericin B is often the first-line pharmacologic therapy for suspected invasive fungal sinusitis. Miconazole is the antifungal of choice for P boydii, (38) and several authors have reported successful treatment with ketoconazole. (12,14,17,19) In 1978, Cosgrove et al theorized that combining amphotericin B with an imidazole antifungal might result in antagonism because the two agents competed for the same binding sites on cell membranes. (39) However, Walsh et al challenged that theory in 1995 when they reported that in vitro studies specific for P boydii showed that the two compounds actually might have a synergistic relationship. (40) More recently, the results of other in vitro studies have supported the use of voriconazole, a new triazole antifungal agent, in the treatment of P boydii infections. (41-43)
Our patient presented with a 4-month history of vague headaches, which are often characteristic of chronic sphenoid sinusitis. (28) He underwent an extensive workup, but the diagnosis was elusive. Only alter orbital apex syndrome had developed was the diagnosis of chronic sinusitis with skull base osteomyelitis made. Even then, the organisms responsible were not known. Pathologic specimens from sphenoid sinus biopsies yielded a mass of fungal hyphae that resembled Aspergillus. It was for this reason that amphotericin B was started. It was not until alter the patient had died that P boydii was grown in cultures of the sphenoid sinus. As discussed, P boydii is typically resistant to amphotericin B, so this patient received inadequate pharmacologic therapy. As for surgical therapy, by the time this patient had been diagnosed, imaging had already demonstrated erosion of a significant part of his anterior skull base and enhancement of the dura of the anterior cranial fossa. An earlier diagnosis and the use of miconazole or voriconazole as the initial therapy might have changed this patient's outcome. However, the literature suggests that patients with invasive P boydii who are immunocompromised have a high mortality rate regardless of therapy.
In conclusion, fungal sinusitis secondary to P boydii infection is rare. When it does occur, it can appear in both immunosuppressed and immunocompetent patients. Although the organism resembles Aspergillus on pathologic examination, P boydii is typically resistant to amphotericin B. Therefore, culture and a definitive identification of the organism are crucial to selecting adequate pharmacologic therapy. Sensitivity testing will help direct antifungal therapy. In general, patients should be treated with a combination of surgery and antifungal therapy, particularly those patients with immunosuppression and fungal invasion. Immunocompetent patients with P boydii fungal sinusitis have a better prognosis, even when invasion is present.
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Dwight D. Bates, MD; J. Whitman Mires, MD
From the Department of Otolaryngology, Wake Forest University School of Medicine, Winston-Salem, N.C.
Reprint requests: J. Whitman Mires. MD, Department of Otolaryngology, Wake Forest University School of Medicine, Medical Center Blvd., Winston-Salem, NC 27157. Phone: (336) 716-5389: fax: (336) 716-3857; e-mail: email@example.com
Originally presented as a poster at the 108th annual meeting of the Triological Society; May 13-16, 2005: Boca Raton, Fla.
Table. Summary of the 26 cases of sinonasal infection with P boydii reported in literature Sinus(es) Immune status Fungal Author Age/sex involved (cause) invasion Gluckman 58/M Maxillary, Compromised Proven et al, (6) 1977 ethmoid, (diabetes) sphenoid Winston 57/F None Compromised Proven et al, 1977 (nasal (leukemia) cavity) Hecht and 20/M Maxillary Compromised Proven Montgomerie, (8) (leukemia) 1978 Mader et al, (9) 33/F Sphenoid Competent Proven 1978 Bark et al, (10) 28/F Maxillary Compromised Unknown 1978 (diabetes) Bryan 47/F Sphenoid Competent Proven et al, (11) 1980 Bloom 57/F Maxillary Compromised Excluded et al, (12) (adrenocortical 1982 Insufficiency) Winn et al, (13) 43/F Maxillary Competent Unknown 1983 Schiess 61/F Maxillary, Compromised Proven et al, (14) 1984 ethmoid, (diabetes) frontal, sphenoid Morgan 45/M Maxillary Competent Proven et al, (15) 1984 Travis 47/M Maxillary Competent Unknown et al, (5) 1985 Washburn 77/F Maxillary Competent Excluded et al, (16) 1988 Salitan 28/F Ethmoid, Competent Unknown et al, (17) sphenoid 1990 Terris and 69/F Sphenoid Competent Excluded Steiniger, (18) 1992 Stamm and 23/F Maxillary, Competent Excluded Frable, (19) ethmoid, 1992 sphenoid Watters and 52/F Ethmoid, Competent Excluded Milford, (20) sphenoid 1993 Grigg 35/F Maxillary, Compromised Proven et al, (21) ethmoid (leukemia) 1993 Meyer 44/M Maxillary, Compromised Suspected, et al, (22) ethmoid, (AIDS) after 1994 frontal, initially sphenoid excluded Fiero 28/F Ethmoid, Competent Excluded et al, (23) sphenoid 1995 Machado 40/M Maxillary Compromised Unknown et al, (24) 1998 (bone marrow transplant) Tadros 33/F Maxillary Compromised Excluded et al, (25) (sickle cell 1998 anemia) Jones 68/M Maxillary, Compromised Suspected et al, (26) ethmoid (leukemia) 1999 Horton 44/M Sphenoid Compromised Suspected et al, (27) (AIDS) 1999 Shaw et al, (28) 85/F Sphenoid Compromised Excluded 2000 (diabetes) Castiglioni 58/F Sphenoid Compromised Not et al, (29) 2002 (post- suspected transplant) Bates and 76/M Sphenoid Compromised Proven Mims, ([dagger]) (diabetes) 2006 Concomitant Author bacteria Treatment Outcome Gluckman Staphylococcus Surgery, * Died of an et al, (6) 1977 aureus, Proteus antifungal unrelated mirabilis therapy cause (amphotericin B) Winston S aureus, Surgery, Died of et al, 1977 P mirabilis antibacterial disease therapy Hecht and Staphylococcus Surgery, Died of Montgomerie, (8) epidermidis, antifungal therapy disease 1978 Enterobacter (5-fluorocytosine, cloacae amphotericin B) Mader et al, (9) Citrobacter Surgery, Infection 1978 freundii antifungal therapy resolved (miconazole) Bark et al, (10) Klebsiella Surgery Unknown 1978 pneumoniae, E cloacae, anaerobic gram- positive rods Bryan None Surgery, Died of et al, (11) antifungal therapy disease 1980 (amphotericin B, then miconazole) Bloom Klebsiella Surgery Infection et al, (12) oxytoca resolved 1982 Winn et al, (13) None Surgery Infection 1983 resolved Schiess K pneumoniae, Surgery, Died of an et al, (14) 1984 S epidermidis antifungal therapy unknown (also Candida (miconazole, then cause albicans) ketoconazole) Morgan C freundii Surgery Infection et al, (15) resolved 1984 Travis C freundii Surgery Infection et al, (5) resolved 1985 Washburn No Surgery Infection et al, (16) 1988 resolved Salitan S aureus Surgery, Infection et al, (17) antifungal therapy resolved 1990 (amphotericin B, switched to miconazole then ketoconazole) Terris and Serratia Surgery Infection Steiniger, (18) liquefasciens resolved 1992 Stamm and None Surgery, Infection Frable, (19) antifungal therapy resolved 1992 (amphotericin B, switched to ketoconazole) Watters and None Surgery Infection Milford, (20) resolved 1993 Grigg None Surgery, Infection et al, (21) antifungal therapy persisted a 1993 (amphotericin B, the most switched to recent miconazole, follow-up rifampin) Meyer S epidermidis Surgery, Infection et al, (22) antifungal therapy recurred; 1994 (ketoconazole) died of a related cause Fiero None Surgery Infection et al, (23) resolved 1995 Machado None Surgery, Died of a et al, (24) 1998 antifungal therapy related (itraconazole) cause Tadros None Surgery Unknown et al, (25) 1998 Jones None Antifungal therapy Died of et al, (26) (amphotericin B, leukemia 1999 itraconazole) Horton None Surgery, Died of an et al, (27) antifungal therapy unknown 1999 (amphotericin B, cause switched to itraconazole) Shaw et al, (28) None Surgery Died, 2000 probably of squamous cell carcinoma Castiglioni None Surgery, Infection et al, (29) 2002 antifungal therapy resolved (miconazole, then itraconazole) Bates and K pneumoniae Antifungal therapy Died of Mims, ([dagger]) (amphotericin B) disease 2006 * Surgical drainage and/or debridement. ([dagger]) Present report.
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|Author:||Mims, J. Whitman|
|Publication:||Ear, Nose and Throat Journal|
|Date:||Nov 1, 2006|
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