through the nose and hence affects the nasal cavity and
then spreads to the surrounding tissues[1].
In 1855, Kurchenmeister described a case of
Mucormycosis in a patient of neoplastic lung on the
basis of its histoplasmology which was probably the
first authentic human case.
In 1876, Furbringer described pulmonary
mucormycosis for the first time which was caused by
Absidia.The first case in humans was reported in 1885
by Paultauf[2].The first publication was done by Gregory
et al, of the first observation of rhino-orbital cerebral
mucormycosis in 1943.The first report was by Harris in
1955 of the first known survivor[4].
According to WHO, the incidence rate of
mucormycosis globally varies from 0.005 to 1.7 per
million population in 2020[7]. A 10-year study from
Tamil Nadu showed an annual incidence of 18.4 cases
per year during 2005–2015[8]. Another study from Tamil
Nadu reported 9.5 cases per year during 2015–2019[8]. A
multicentre study across India reported 465 cases from
12 centres over 21 months; the study reported an annual
incidence of 22 cases per year, and an average of 38.8
cases for each participating centre[8]. Chakrabarti et al
showed an increasing trend of mucormycosis, with an
annual incidence of 12.9 cases per year during 1990–
1999, 35.6 cases per year during 2000–2004, and
50 cases per year during 2006–2007. The overall
numbers increased from 25 cases per year (1990–2007)
to 89 cases per year (2013–2015)[9]. Though invasive
aspergillosis is given importance among invasive
mould infections in intensive-care units (ICUs), a
multicentre s tudy in Indian ICUs reported
mucormycosis in a considerable (14%) number of
patients[9]. Without population-based estimates, it is
difficult to determine the exact incidence and
prevalence of mucormycosis in the Indian population.
The computational-model-based method estimated a
prevalence of 14 cases per 100,000 individuals in India.
In India, prevalence of mucormycosis is about 80 times
higher than the prevalence in developed countries[7].
In India, Diabetes mellitus has been the most
common risk factor linked with mucormycosis[9]. Other
causes include haematological malignancy and
chemotherapy, haematopoietic stem cells, and solid-
organ transplant recipients on immunosuppressive
therapy, with iron overload, on peritoneal dialysis,
extensive skin injury, human immunodeficiency virus
(HIV) infection, and voriconazole therapy[10].
Along with these, COVID-19 disease has a
propensity to cause extensive pulmonary disease and
subsequent alveolo-interstitial pathology. This by itself
may predispose to invasive fungal infections of the
airways including the sinuses and the lungs.
Furthermore, there is an alteration of the innate
immunity due to COVID-19-associated immune
dysregulation characterized by decreased T cells,
including CD4 and CD8 cells[11]. Other factors like
steroid administration, immunomodulating drugs like
tocilizumab, and high doses of Vitamin C, oxygen
therapy, and prolonged hospitalization predispose the
development of mucormycosis.
Initial clinical assessment calls for an
investigation; MRI being the modality of choice to
evaluate the extent of disease and prognostication. Next
in line being CT although it has been observed that
CBCT is one of the most underrated imaging modalities
in the early diagnosis of mucormycosis as evidenced by
the paucity of literature. As of late, CBCT has been
considered as the examination of choice in various
instances, since it gives high resolution imaging,
diagnostic consistency and risk benefit assessment[6].
In the case mentioned in this report, we
evaluated the patient through proper history, assessing
the clinical signs and symptoms, subjecting the patient
to available modality i.e. CBCT and applying the
diagnostic criteria based on CBCT findings to
formulate a diagnosis.
The clinical findings included gingival
enlargement, diffuse swelling involving hard palate and
segmental mobility. In severe cases, a necrosed
ulcerative area forms over the palate owing to the
thrombosis which eventually causes exposure of the
non-vital bone[10].
CBCT images show loss of cortical bone along
with obliteration of right and left maxillary sinus
suggestive of invasion of sinus lumen.
In cases where the infection has spread through
the other paranasal sinuses, ocular involvement takes
place through the thin lamina papyracea of the ethmoid
bone into the orbit resulting in rhino-sino-orbital
mucormycosis[10].
The treatment for mucormycosis infections
involves the utilization of Amphotericin B, which is the
initial FDA-approved drug for this purpose.
Amphoterecin B is available in different lipid
formulations, including liposomal preparation, lipid
complex, and colloidal dispersion. These formulations
enhance the effectiveness of the drug and improve its
administration to the affected areas, thereby assisting in
the treatment of mucormycosis infections, administered
in the dose of 10 mg/kg/day.[12] A dosage of 5mg/kg/day
is recommended in COVID-19 associated Mucormy-
cosis. An oral suspension of Posaconazole
800mg/24hrs in 2 divided doses is advised for 12-13
weeks[13].