Pathogenesis, and Risk Factors



Fig. 1
Risk factors for invasive fungal sinusitis – many of them are interrelated



Documented mucormycosis is at least five to ten times less common as compared to other mold infections such as Aspergillosis, making it difficult for inexperienced personnel to identify the infection early [3]. As the pathophysiology, mode of acquisition, and underlying patient risk factors for mucormycosis are similar to aspergillosis, clinical distinction between the two entities is difficult [36]. Both infections are acquired primarily through inhalation of fungal spores, which are ubiquitous in the environment, leading to sinopulmonary disease [3739] (Fig. 2). However, some scenarios, risk factors, and elements of clinical and radiological features could prompt to a high index of suspicion for incipient mucormycosis [18, 35] (Table 1).

A316236_1_En_3_Fig2_HTML.jpg


Fig. 2
Pathophysiology of invasive fungal sinusitis (Based on Pathophysiology of invasive pulmonary mucormycosis: Kontoyiannis and Lewis [36])



Table 1
Factors favoring mucormycosis over aspergillosis (Kontoyiannis and Lewis [36])

















































Clues

Comments

Epidemiology and host clues
 

Institution with high rates of mucormycosis

Unique geographic exposures vs. institution-specific differences in immunosuppression and anti-infective practices

Iron overload

Most reliable method of diagnosis unclear

Hyperglycemia with or without diabetes mellitus

Degree and duration undefined

Prior voriconazole or echinocandin use

The magnitude and specificity of such association are debatable

Clinical, radiologic, and laboratory clues
 

Community-acquired sinusitis

Pansinusitis or ethmoid involvement are important clinical clues of mucormycosis

Oral or necrotic lesions on hard palate or turbinates
 

Chest wall cellulitis adjacent to lung infarct

Mucormycosis can spread across tissue planes

Acute vascular event (e.g., myocardial infarct, GI bleeding)

Resulting from acute hemorrhagic infarct caused by Mucorales

Reverse halo sign on CXR or CT

Halo sign is as common in invasive pulmonary mucor as in invasive pulmonary aspergillosis

Presumed (by CT findings) fungal pneumonia with adequate voriconazole levels
 

Presumed (by CT findings) fungal pneumonia with repetitively negative galactomannan and G-glucan serum levels
 


References



1.

Veress B, Malik OA, Tayeb AA, El Daoud S, El Mahgoub S, El Hassan AM. Further observations on the primary paranasal Aspergillus granuloma in Sudan. Am J Trop Med Hyg. 1973;22:765–72.PubMed


2.

Chakrabarti A, Sharma SC. Paranasal sinus mycoses. Indian J Chest Dis Allied Sci. 2000;42:293–304.PubMed


3.

Chamilos G, Luna M, Lewis RE, et al. Invasive fungal infections in patients with hematologic malignancies in a tertiary care cancer center: an autopsy study over a 15 year period (1989–2003). Haematologica. 2006;91(7):986–9.PubMed


4.

Kontoyiannis DP, Wessel VC, Bodey GP, Rolston VI. Zygomycosis in the 1990s in a tertiary care cancer center. Clin Infect Dis. 2000;30:851–6.PubMedCrossRef


5.

Talmi YP, Goldschmeid-Reouven A, Bakon M, et al. Rhino-orbital and rhino-orbito-cerebral mucormycosis. Otolaryngol Head Neck Surg. 2002;127:22–31.PubMedCrossRef


6.

Funada H, Matsuda T. Pulmonary mucormycosis in a hematology ward. Intern Med. 1996;35:540–4.PubMedCrossRef


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Chakrabarti A, Sharma SC, Chander J. Epidemiology and pathogenesis of paranasal sinus mycoses. Otolaryngol Head Neck Surg. 1992;107:745–50.PubMed


8.

Prabhu RM, Patel R. Mucormycosis and entomophthoramycosis: a review of the clinical manifestations, diagnosis and treatment. Clin Microbiol Infect. 2004;10 Suppl 1:31–47.PubMedCrossRef

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Mar 26, 2017 | Posted by in OTOLARYNGOLOGY | Comments Off on Pathogenesis, and Risk Factors

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