Old Disease, New Faces; Mucormycosis in Post SARS Covid-19 Era: A Review

International Journal of Dental Science and Innovative Research (IJDSIR) IJDSIR : Dental Publication Service Available Online at:www.ijdsir.com Volume – 8, Issue – 5, September – 2025, Page No. : 189 – 196 Corresponding Author: Dr. Avni Shrivastava, ijdsir, Volume – 8 Issue - 5, Page No. : 189 – 196 Page189 ISSN: 2581-5989 PubMed - National Library of Medicine - ID: 101738774 Old Disease, New Faces; Mucormycosis in Post SARS Covid-19 Era: A Review 1Dr. Avni Shrivastava, Post Graduate Student, Department of Oral Medicine and Radiology, Hitkarini Dental College and Hospital, Jabalpur. 2Dr. Ankur Kakkad, Professor, Department of Oral Medicine and Radiology, Hitkarini Dental College and Hospital, Jabalpur. 3Dr. Ankit Dhimole, Associate Professor, Department of Oral Medicine and Radiology, Hitkarini Dental College and Hospital, Jabalpur. 4Dr. Tamanna Yadav, Post Graduate Student, Department of Oral Medicine and Radiology, Hitkarini Dental College and Hospital, Jabalpur Corresponding Author: Dr. Avni Shrivastava, Post Graduate Student, Department of Oral Medicine and Radiology, Hitkarini Dental College and Hospital, Jabalpur. Citation of this Article: Dr. Avni Shrivastava, Dr. Ankur Kakkad, Dr. Ankit Dhimole, Dr. Tamanna Yadav, “Old Disease, New Faces; Mucormycosis in Post SARS Covid-19 Era: A Review”, IJDSIRSeptember – 2025, Volume – 8, Issue – 5, P. No. 189 – 196. Copyright: © 2025, Dr. Avni Shrivastava, et al. This is an open access journal and article distributed under the terms of the creative common’s attribution non-commercial License. Which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given, and the new creations are licensed under the identical terms. Type of Publication: Review Article Conflicts of Interest: Nil Abstract Mucormycosis is a severe yet uncommon angioinvasive fungal infection that progresses rapidly, making early diagnosis and treatment essential to reduce its high mortality and morbidity rates. The disease arises primarily from inhalation of filamentous (hyphal) fungal spores, particularly in immunocompromised individuals. This review highlights the etiopathogenesis of mucormycosis, the fatal consequences of rhino cerebral mucormycosis, its complex association with COVID-19, and the latest advances in diagnostic and therapeutic approaches. Keywords: Mucormycosis, Oral manifestations, SARS COVID-19. Introduction Mucormycosis, also referred to as phycomycosis or “black fungus” (formerly known as zygomycosis), is a potentially lethal opportunistic fungal infection. It is caused by filamentous molds belonging to the orders Mucorales and Entomophthorales of the zygomycete family, which are capable of producing various types of infections 1. These fungi are commonly found in soil, decaying organic matter (such as rotting fruits and vegetables), and animal manure. However, they rarely infect healthy Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 Page190 individuals and are not transmitted from person to person2. During the COVID-19 pandemic, a strong association was observed between mucormycosis and COVID-19, particularly in India, where cases increased markedly. This relationship is believed to be linked to immune suppression during COVID-19 infection and the widespread use of glucocorticoids in treatment 3. Characterized by its rapid progression and high mortality rate, mucormycosis can manifest in various forms, including rhinocerebral, pulmonary, gastrointestinal, cutaneous, and disseminated infections. Prompt diagnosis and treatment are crucial to prevent severe morbidity and mortality. However, diagnosis is often delayed due to its nonspecific clinical presentation and limited awareness among healthcare professionals. This review aims to provide a comprehensive overview of mucormycosis, including its clinical manifestations, diagnosis, treatment options, and current challenges in management. By understanding this deadly fungal infection, healthcare professionals can improve patient outcomes and save lives 2. Historic Background The first case of mucormycosis was reported in 1885 by German pathologist Paltauf, who described it as Mycosis Mucorina4 The 1980s and 1990s saw a rise in cases, particularly among immunocompromised individuals3. A study in France revealed an annual increase of 7.4% in incidence 5. Globally, mucormycosis has been reported with indications of seasonal variation in Mucorales infections 6. The rise has been perceived globally, but it is very high in the Asian continent. Though diabetes mellitus over shadow all other risk factors in Asia. Mucormycosis is found to be predisposed in comorbidity or in the nondiabetic patients of COVID19 especially in those who were at high dosage of steroids for a longer period of time or on ventilator support. In a report, it is observed that among all the patients of COVID-19 associated mucormycosis (CAM) about 80.4-96.7%haddiabetes mellitus 4. Etiopathogenesis Mucorales invade deep tissues through ingestion, inhalation, or percutaneous inoculation of spores. In healthy individuals, the first line of defense—oxidative metabolites and cationic peptides—can typically neutralize these spores 7. Risk Factors The infection is more likely in individuals with uncontrolled diabetes mellitus, particularly ketoacidosis, steroid use, extremes of age, neutropenia (especially in hematological malignancies), AIDS, renal failure, organ or stem cell transplantation, iron overload, skin trauma, broad-spectrum antibiotic use, intravenous drug abuse, prolonged voriconazole prophylaxis for aspergillosis, malnutrition7 .In diabetic patients, mucormycosis becomes highly destructive due to the increased availability of nutrients and reduced immune defense [8]. Proposed mechanisms include, low serum inhibitory activity against rhizopus species, enhanced iron availability in acidic conditions, reduced ability of pulmonary macrophages to inhibit rhizopus spore germination9-11. Rhizopus produces ketone reductase, which enables survival in high-glucose, acidic environments11. In patients with diabetic ketoacidosis (DKA), mucormycosis of all types can develop 11–14. Neutrophils, essential in defense against Mucorales, have impaired function in DKA13,16. The acidic state accelerates fungal invasion17, while free iron availability and reduced transferrin binding create favorable conditions for fungal Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 Page191 proliferation18. Before amphotericin B and surgical interventions, mortality exceeded 90% 19. Patients with neutropenia or defective phagocytosis are at greater risk, although this is less evident in AIDS patients, suggesting T lymphocytes play little role in halting fungal proliferation compared to neutrophils 20. Prolonged voriconazole therapy, particularly in patients with hematologic malignancies or transplants, also increases risk 21–25. Cases have also been reported in individuals without identifiable immune deficiencies, often linked to burns, trauma, or iatrogenic factors 26–28. Oral Manifestation with Rhino Cerebral Mucormycosis (ROCM) Mucormycosis can present in two broad categories: Superficial vs. Visceral: Superficial: external ear, skin, nails; Visceral: pulmonary, gastrointestinal, rhino cerebral. Localized vs. Disseminated: Spores enter through the skin or respiratory tract—for instance, via contaminated food or needles 29,30 ROCM is the most frequent form in diabetic patients but also occurs in individuals with malignancies, transplant recipients, and other immunocompromised hosts. The infection begins when spores reach the paranasal sinuses, then spread rapidly into surrounding tissues. The fungus can invade the palate, sphenoid sinus, cavernous sinus, or even the brain via the orbital apex or ethmoid bone. Vascular invasion may result in hematogenous dissemination or mycotic aneurysm formation 31. Clinical Features Initial symptoms resemble sinusitis or periorbital cellulitis, including: facial pain or numbness, periorbital swelling, blurred vision. Progressive features include: cranial nerve palsies, orbital inflammation, edema, proptosis, blepharoptosis, ophthalmoplegia (internal/external), severe headache, acute vision loss A hallmark sign is the presence of a black necrotic eschar, though its absence does not rule out the disease. fever may be absent in half of patients. leukocytosis is typical if bone marrow function remains intact 32. Role of Mucormycosis in Covid-19 COVID-19 presents with fever, hypoxia, altered osmolarity, and breathlessness33. Many recovered COVID-19 patients subsequently developed mucormycosis, with the fungus spreading to the sinuses, lungs, orbit, and even intracranial structures 33. The immunosuppressive environment created by COVID-19, along with widespread corticosteroid use, significantly increases risk. Patients most vulnerable include diabetics, neutropenic individuals, transplant recipients, and those with hematologic malignancies 34. Studies indicate diabetic patients are especially prone to COVID-19–associated mucormycosis 37,35. Mechanisms linking diabetes with severe COVID-19 include: Impaired viral clearance, T-cell dysfunction, Cytokine storm exaggeration, Immunosuppression 33. Hyperglycemia worsens cytokine storms by damaging endothelial cells and causing multi-organ injury. In diabetic ketoacidosis, acidic pH and excess free ferric ions further facilitate Mucorales growth and invasion 33. Steroid therapy, while beneficial against COVID-19– induced inflammation, reduces white blood cell and Thelper cell activity, weakens immunity, and increases blood sugar levels, thereby creating a favourable environment for fungal invasion. Prolonged oxygen therapy and use of humidifiers/ventilators may add to the risk 36. Although only limited case reports exist, the available evidence strongly supports these mechanisms as key contributors to the surge in mucormycosis among COVID-19 patients 36. Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Page192 Challenges in Managing Mucormycosis Mucormycosis carries a mortality rate of nearly 50%. COVID-19 patients, particularly those requiring oxygen therapy, face an elevated risk. Inhalation of spores in immunocompromised hosts leads to colonization, vascular invasion, and widespread tissue damage. Uncontrolled diabetes remains the single most important risk factor due to high blood glucose levels and compromised immunity. Additional environmental factors such as warm, humid conditions and contaminated oxygen devices further promote infection. Delayed diagnosis and treatment dramatically worsen outcomes 37. Radiographic Features Sinus opacification is often accompanied by patchy erosion of the bony sinus walls. In cases of cavernous sinus thrombophlebitis, mucormycosis may present with the “black turbinate sign,” which refers to a nonenhancing area of mucosa on MRI 38. CT or MRI imaging may reveal thickened mucosa, opacified sinuses, congested extraocular muscles, orbital apex crowding, proptosis, and optic nerve inflammation 39. In pulmonary mucormycosis, micro-nodules and multiple additional nodules may be detected, consistent with findings reported by Chamilos et al 40,41. Histopathological Features Histological examination of infected tissue typically reveals extensive necrosis with numerous broad, ribbonlike, pale-staining, non-septate hyphae branching at right or obtuse angles. Round or ovoid sporangia are commonly observed in cultures. The hyphae are thinwalled, usually non-septate, with irregular branching and occasional bulbous swelling, measuring 3–25 μm in diameter. Necrotic tissue with hyphae often demonstrates angio-invasion and infarction. In non-granulocytopenic patients, neutrophilic infiltration is seen, and chronic cases may show granuloma formation. Gomori Methenamine Silver (Grocott) and Periodic Acid-Schiff (PAS) stains are preferred for identification 42. Diagnostic Methods Diagnosis requires careful clinical assessment, supported by MRI and early CT imaging, as well as cytological and histological evaluations. Microbiological methods, molecular detection,43 and host factor identification play a critical role in assessing the risk of invasive mucormycosis. Laboratory techniques include PAS staining, direct microscopy, calcofluor staining, histopathology, Gomori methenamine silver stain, culture, molecular assays, and fluorescent in situ hybridization. According to Kontoyiannis et al., challenges in diagnosis arise due to the nonspecific clinical presentation and occult dissemination of the disease. Tissue-based analysis remains the gold standard for confirmation 22. Differential Diagnosis Mucormycosis should be distinguished from maxillary sinus neoplasms, aspergillosis, soft tissue infarction, radionecrosis, and other deep fungal infections 44. Treatment Effective management involves prompt diagnosis, surgical debridement, antifungal therapy, and adjunctive options such as hyperbaric oxygen, recombinant cytokines, granulocyte transfusion, and prosthetic obturators. Spellberg et al. noted that monotherapy carries high mortality rates, particularly in haematology patients, and recommend combination therapy for improved outcomes 45. Common antifungal regimens include Amphotericin B deoxycholate, liposomal Amphotericin B (5–10 mg/kg), Amphotericin B lipid complex, Amphotericin B colloidal dispersion, and Posaconazole (400 mg twice daily), along with management of underlying conditions. Second-line Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 Page193 therapy may involve combinations such as caspofungin with lipid Amphotericin B or lipid Amphotericin B with Posaconazole. Deferasirox is not recommended. Surgical intervention should be considered for soft tissue, cerebral, localized pulmonary, and rhino-orbito forms of mucormycosis 46. Prognosis and Morbidity Prognosis depends on disease extent and timely initiation of treatment. In rhino-cerebral mucormycosis, survival is about 75% in patients without systemic disease but drops to ~20% in those with comorbidities. Pulmonary mucormycosis is often fatal 47. Survival rates vary by site: Rhino-cerebral: 45%, Focal cerebral: 33%, Pulmonary: 36%, Sinusitis (without cerebral involvement): 87%, Cutaneous isolated: 90%, Disseminated: 16%, Gastrointestinal: 10%. Better outcomes are associated with low baseline serum iron/ferritin levels, absence of neutropenia, and malignancies not complicated by infection 48. Conclusion COVID-19 has created global health challenges, and its treatment and complications have predisposed patients to secondary fungal infections like mucormycosis. This angioinvasive fungus, commonly found in soil, plants, dung, and decaying produce, becomes life-threatening when inhaled by immunocompromised hosts, particularly those with diabetes and those receiving corticosteroid therapy. Once inhaled, fungal spores invade blood vessels, causing thrombosis, tissue necrosis, and infarction. Highrisk groups include individuals with diabetic ketoacidosis, neutropenia, excess iron levels, and steroidinduced hyperglycaemia, all of which reduce WBC and T-cell activity and worsen cytokine storms. To combat this fatal infection, timely diagnosis, antifungal therapy, surgical management when required, and a multidisciplinary treatment approach are essential. Future research must focus on clarifying the mechanisms of mucormycosis in COVID-19 patients and developing effective strategies for prevention and treatment. Diagnostic vigilance is crucial, particularly in COVID19–positive and immunosuppressed individuals. Reference 1. Dyer O. Covid-19: India sees record deaths as black fungus spreads fear. BMJ. 2021;373: n1238. doi: 10.1136/bmj. n1238. PMID 33985993. 2. Where Mucormycosis Comes From. 2021. Retrieved: 2021; Available from: www.cdc.gov. 3. Mucormycosis. NORD (National Organization for Rare Disorders). Archived from the original on 2021. Retrieved: 2021. 4. Mohammadi R, Nazeri M, Sayedayn SM, Ehteram H. A successful treatment of rhinocerebral mucormycosis due to Rhizopus oryzae. Journal of research in medical sciences: The Official Journal of Isfahan University of Medical Sciences, 2014; 19(1): 72. 5. Roden MM, Zaoutis TE, Buchanan WL, Knudsen TA, Sarkisova TA, Schaufele RL, Sein M, Sein T, Chiou CC, Chu JH, Kontoyiannis DP. Epidemiology and outcome of zygomycosis: a review of 929 reported cases. Clinical Infectious Diseases, 2005; 41(5): 634-53. 6. Bitar D, Van Cauteren D, Lanternier F et al. Increasing incidence of zygomycosis (mucormycosis), France, 1997–2006. Emerg Infect Dis., 2009; 15: 1395–1401. 7. Petrikkos G, Skiada A, Lortholary O, Roilides E, Walsh TJ, Kontoyiannis DP. Epidemiology and clinical manifestations of mucormycosis. Clinical Infectious Diseases, 2012; 54(suppl_1): S23-34. Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 Page194 8. Waldorf AR. Pulmonary defense mechanisms against opportunistic fungal pathogens. Immunol Ser., 1989; 47: 243–271 9. Rammaert B, Lanternier F, Poirיe S, Kania R, Lortholary O. Diabetes and mucormycosis: a complex interplay. Diabetes & metabolism, 2012; 38 (3): 193-204. 10. Meyer BR, Wormser G, Hirschan SZ, et al. Rhinocerebral mucormycosis: premortem diagnosis and therapy. Arch. Intern. Med., 1979; 139: 557. 11. Gale GR, Welch AM. Studies of opportunistic fungi. I. Inhibition of Rhizopus oryzae by human serum. Am. J. Med. Sci., 1961; 241: 604–12. 12. Waldorf AR, Ruderman N, Diamond RD. Specific susceptibility to mucormycosis in murine diabetes and bronchoalveolar macrophage defense against Rhizopus. J. Clin. Invest., 1984; 74: 150 60. 13. Tedder M, Spratt JA, Anstadt MP, Hegde SS, Tedder SD, Lowe JE. Pulmonary mucormycosis: results of medical and surgical therapy. Ann. Thorac. Surg., 1994; 57(4): 104450. 14. Joshi N, Caputo GM, Weitekamp MR, Karchmer AW. Infections in patients with diabetes mellitus. N. Engl. J Med., 1999; 341(25): 190612. 15. Bhansali A, Sharma A, Kashyap A, Gupta A, Dash RJ. Mucor endophthalmitis. Acta Ophthalmol Scand., 2001; 79(1): 8890. 16. Tsaousis G, Koutsouri A, Gatsiou C, Paniara O, Peppas C, Chalevelakis G. Liver and brain mucormycosis in a diabetic patient type II successfully treated with liposomal amphotericin B. Scand. J. Infect. Dis., 2000; 32(3): 3357. 17. Waldorf AR, Levitz SM, Diamond RD. In vivo bronchoalveolar macrophage defense against Rhizopus oryzae and Aspergillus fumigatus. J. Infect. Dis., 1984; 150(5): 752-60. 18. Artis WM, Fountain JA, Delcher HK. A mechanism of susceptibility to mucormycosis in diabetic ketoacidosis: transferrin and iron availability. Diabetes, 1982; 31: 109–14. 19. Cohen SG, Greenberg MS. Rhinomaxillary mucormycosis in a kidney transplant patient. Oral Surg. Oral Med. Pathol., 1980; 50: 33–8. 20. Marchevskey AM, Bottone EJ, Geller SA. The changing spectrum of disease etiology and diagnosis of mucormycosis. Human Pathology, 1980; 11: 457. 21. Sugar AM. Agents of mucormycosis and related species. In: Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious diseases. 6th ed. Philadelphia, PA: Elsevier, 2005; 2979. 22. Kontoyiannis DP, Lionakis MS, Lewis RE, et al. Zygomycoses in a tertiary-care cancer center in the era of Aspergillus-active antifungaltherapy: a casecontrol observational study of 27 recent cases. J. Infect. Dis., 2005; 191:1350–60. 23. Oren I. Breakthrough mucormycosis during empirical voriconazole therapy in febrile patients with neutropenia. Clin Infect Dis., 2005; 40: 7701. 24. Trifilio SM, Bennett CL, Yarnold PR, et al. Breakthrough mucormycosis after voriconazole administration among patients with hema-tologic malignancies who receive hematopoietic stem-cell transplants or intensive chemo-therapy. Bone Marrow Transplant, 2007; 39: 425–9. 25. Wingard JR, Carter SL, Walsh TJ, et al. Randomized, double-blind trial of fluconazole versus voriconazole for prevention of invasive-fungal infection after allogeneic hematopoietic cell transplantation. Blood, 2010; 116: 5111–18. 26. Marks DI, Pagliuca A, Kibbler CC, et al. Voriconazole versus itraconazole for antifungal prophylaxis Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 Page195 following allogeneic haematopo-ieticstem-cell transplantation. Br. J. Haem., 2011; 155: 318–27. 27. Torres-Narbona M, Guinea J, Martinez-Alarcon J, et al. Impact of mucormycosis on microbiology overload: a survey study in Spain. J. Clin. Microbiol., 2007; 45: 2051–3. 28. Cheng VC, Chan JF, Ngan AH, et al. Outbreak of intestinal infection due to Rhizopus microsporus. J. Clin. Microbiol., 2009; 47: 2834–43. 29. Skiada A, Petrikkos G. Cutaneous mucormycosis. Clin. Microbiol. Infect., 2009; 15(Suppl 5): 41–5. 30. Spellberg B, Edwards J Jr, Ibrahim A. Novel perspectives on mucormycosis: pathophysiology, presentation, and management. Clin. Microbiol. Rev., 2005; 18: 556–569. 31. Perlroth J, Choi B et al. Nosocomial fungal infections: epidemiology. Diagnosis and treatment, Med Mycol, 2007; 45:321-46. 32. Antoniadou A. Outbreaks of mucormycosis in hospitals, Clin Microbiol Infect, 2009;15 (5):55-9. 33. Balachandar V., Mahalaxmi I., Devi S.M., Kaavya J., Kumar N.S., Laldinmawii G., Arul N., Reddy S.J.K., Sivaprakash P., Kanchana S. Follow-up studies in COVID-19 recovered patients-is it mandatory? Sci. Total Environ. 2020:139021. doi: 10.1016/ j.scitotenv.2020.139021 34. Binder U., Maurer E., Lass‐Flörl C. Mucormycosis– from the pathogens to the disease. Clin. Microbiol. Infect. 2014;20:60–66. doi: 10.1111/ 1469-0691. 12566. 35. Ahmadikia K., Hashemi S.J., Khodavaisy S., Getso M.I., Alijani N., Badali H., Mirhendi H., Salehi M., Tabari A., MohammadiArdehali M. The double‐ edged sword of systemic corticosteroid therapy in viral pneumonia: a case report and comparative review of influenza‐associated mucormycosis versus COVID‐19 associated mucormycosis. Mycoses. 2021 doi: 10.1111/myc.13256 36. Kinoshita M., Sato K., Vellingiri B., Green S.J., Tanaka M. Inverse association between hypertension treatment and COVID-19 prevalence in Japan. Int. J. Infect. Dis. 2021 doi: 10.1016/j.ijid.2021.05.071. 37. Mehta S., Pandey A. Rhino-orbital mucormycosis associated with COVID-19. Cureus. 2020;12 doi: 10.7759/cureus.10726. S26669919(21)00030-0. 38. Safder S, Carpenter JS, Roberts TD, Bailey N. The “black turbinate” sign: an early MR imaging finding Of nasal mucormycosis. AJNR. Amer. J. Neuroradiol., 2010; 31: 771-774. 39. Rogers WD. Facial paralysis and epistaxis in a diabetic: a typical presentation for rhinocerebral mucormycosis. Ann. Emerg. Med., 1984; 13: 560 –1 40. Chamilos G, Marom EM, Lewis RE, Lionakis MS, Kontoyiannis DP. Predictors of pulmonary zygomycosis versus invasive pulmonary aspergillosis in patients with cancer. Clin. Infect. Dis., 2005; 41: 60-66. 41. Hamilos G, Samonis G, Kontoyiannis DP. Pulmonary mucormycosis. Semin. Respir. Crit. Care Med., 2011; 32: 693–702 42. Jensen HE, Salonen J, Ekfors TO. The use of immunohistochemistry to improve sensitivity and specificity in the diagnosis of systemic mycoses in patients with haematological malignancies. J. Pathol.,1997; 181(1): 100-5 43. Walsh TJ, Gamaletsou MN, McGinnis MR, Hayden RT, Kontoyiannis DP. Early clinical and laboratory diagnosis of invasive pulmonary, extrapulmonary, and disseminated mucormycosis (zygomycosis). Clinical Infectious Diseases, 2012; 54(suppl 1):S55-60. Dr. Avni Shrivastava, et al. International Journal of Dental Science and Innovative Research (IJDSIR) ©2025 IJDSIR, All Rights Reserved Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 Page196 44. Sciubba JJ, Regezi JA, Rogers RS. PDQ oral disease: diagnosis and treatment. PMPH-USA; 2002. 45. Spellberg B, Ibrahim A, Rolides E, Lewis RE, Lortholary O, Petrikkos G, Kontoyiannis DP, Walsh TJ. Combination therapy for mucormycosis: why, what, and how?. Clinical infectious diseases, 2012; 54(suppl 1): S73-8. 46. Skiada A, Lanternier F, Groll AH, Pagano L, Zimmerli S, Herbrecht R, Lortholary O, Petrikkos GL. Diagnosis and treatment of mucormycosis in patients with haematological malignancies: guidelines from the 3rd European Conference on Infections in Leukemia (ECIL 3). Haematological, 2013; 98(4): 492-504. 47. Petrikkos G, Skiada A, Sambatakou H et al. Mucormycosis:ten-year experience at a tertiary-care center in Greece. Eur. J. Clin. Microbiol. Infect Dis., 2003; 22: 753–756. 48. Nithyanandam S, Jacob MS, Battu RR, Thomas RK, Correa MA, D’Souza O. Rhino-orbito-cerebral mucormycosis. A retrospective analysis of clinical features and treatment outcomes. Ind. J. Ophthalmol., 2003; 51: 231–236