1. Mycotic diseases of the paranasal
sinuses
Mycotic diseases of the paranasal sinuses range from an indolent infection in an otherwise normal
person, to a lethal fulminant infection in an immunocompromised individual.
Based on histopathological finding & clinical presentation, fungal sinusitis is now classified into three
categories: invasive sinusitis, noninvasive sinusitis & allergic fungal sinusitis.
Invasive fungal sinusitis
Definition : invasive fungal sinus disease can be subdivided into the following three syndromes:
acute fulminant invasive sinusitis,chronic invasive sinusitis & chronic granulomatous invasive
sinusitis(paranasal granuloma).
1) Acute invasive sinusitis: acute fulminating (invasive) fungal sinusitis is a rapidly progressive
disease that is most commonly seen in immunocompromised individuals or diabetes. The
infection can spread from the nasal mucosa & sinus into orbit & brain. The aetiological
agents have a predilection for vascular invasion causing thrombosis, infarction& ischaemic
necrosis of tissue. Blood vessels invasion is seen histologically.
2) Chronic invasive sinusitis: chronic (invasive) sinusitis is a slowly progressive disease that is
seen in both immunocompromised or immunocompetent individuals. This condition may be
begin as a paranasal sinus fungus ball.(non-invasive fungal sinusitis) then become invasive,
perhaps as result of the immunosuppression associated with diabetes mellitus or
corticosteroid treatment. If untreated, the infection can spread to invade adjacent
structures including the orbit & brain. The most common agent are Aspergillus, bipolaris&
curvularis species. Itraconazole 100mg/bd result in remineralization of the eroded skull
bone.
3) Chronic granulomatous invasive sinusitis: granulomatous invasive fungal sinustitis is a
slowly progressive disease that occurs in immunocompromised persons who often have had
chronic sinusitis. There is profuse fungal growth with localised tissue invasion, noncaseating
granulomas with giant cells. The granulomatous response is often intense enough to cause
pressure necrosis of bone & can spread to orbit & brain. Most cases reported in North
Africa. Most common agent is A.flavus. surgical removal of granuloma is difficult. Medical
treatment itraconazole 100mg/bd.
Aetiological agents
Many different organisms have been implicated as aetiological agents of invasive fungal sinusitis.
However the commonest causes of acute fulminant sinusitis are moulds belonging to the order
mucorales. Others less frequent causes aspergillus species.
Many of these organisms are ubiquitous in the environment, being found in the air, in the soil& on
decomposing organic matter, others are plant poathogens.

2. Epidemiology
The aetiological agents that infection will occur following inhalation of fungal spores largely
depends on host factors. Prolonged neutropenia & metabolic acidosis are well recognised as an
important risk factors for rhinocerebral mucormycosis & fulminant aspergillus sinusitis among
patients with haematological malignancies & diabetes mellitus. Others contributing factors include
the use of corticosteroids & AIDS.
Clinical manifestations
In immunocompromised persons, acute invasive fungal sinusitis presents with fever, unilateral facial
swelling, unilateral heahache, nasal obstruction or pain & a serosanguinous nasal discharge. Necrotic
black lesions on the hard palate or nasal turbinate are a characteristic diagnostic sign.
Many patients present with a history of nasal obstruction & chronic sinusitis. Thick nasal polyposis &
thick purulent mucus are common. If infection spread from ethmoid sinuses into orbit, the orbital
apex syndrome is a common clinical presentation.
Diagnosis
Plain x-ray are insensitive & donot allow distinction between bacterial & fungal infections.
CT scanning can be used to assess the extent of bone destruction. MRI is not superior to CT.
1) The commonest finding of acute invasive fungal sinusitis include involvement of several
sinuses but with unilateral predilection, no air-fluid level, thickening of sinus lining&
destruction of bone.
2) In patient with chronic invasive sinusitis, CT scan shows a hyperdense mass (owing to a
dense accumulation of fungal hyphae) within the involved sinus with erosion of sinus wall.
3) The most common CT scan finding in patient with granulomatous invasive fungal
sinusitis(paranasal granuloma) are opacification of ethmoid, maxillary or all sinuses,
together with erosion of bone.
Local biopsy & histopathological examination & culture of tissue or sinus contents confirm the
clinical & radiological diagnosis.
Microscopic examination of smear ( potassium hydroxide preparation ) material taken from necrotic
lesions.
Isolation of aetiological agent in culture is essential for the species of fungus involved to be
identified.
Management
If treatment of acute invasive fungal sinusitis is to be successful, a prompt diagnosis is essential.
Correction of acidosis is essential & immunosupresive drugs should be reduced in dose. Infected &
necrotic material removed immediately. In acute fulminant fungal sinusitis with invasion of blood
vessels amphotericin B has been considered the drug of choice. Newer lipid based formulation of the
drug, in high doses of liposomal amphotericin B (10-15mg/kg per day) should be considered the first

3. line of treatment. This should be continued until the patient recovers ,at least until the progression
of disease ceases& underlying disorder is well controlled. Patient with amphotericin B should be
monitored for signs of renal damage. Other treatment options are administration of hyperboric
oxygen, iron chelators & cytokine.
Chronic invasive sinusitis, a histological diagnosis is needed to exclude blood vessel invasion in acute
fulminant fungal sinusitis. Extensive surgical debridement with removal of all necrotic material
combined with antifungal treatment has been recommoned. The optimum duration of itraconazole
200mg/bd has not been defined. The role of newer triazole antifungal agents such as itraconazole,
voriconazole& posaconazole, is unclear but promising. There is evidence that long-term treatment
can reduce the rate of recurrence following surgical resection or cure the condition on its own.
Itraconazole 200mg/bd has made surgery unnecessary in most cases. It is important to exclude
fulminant acute sinusitis by histology(invasion of blood vessels).
Noninvasive fungal sinusitis
Definition : a paranasal sinus ball(or sinus mycetoma) is a chronic noninvasive fungal infection that is
seen in immunocompetent persons. However, if immunocompromise should occur, then the
condition may become invasive & life-threatening. Fungus ball consists of a dense mass of fungal
hyphae. They are sometimes found in the sinus cavities of patients undergoing investigation for
chronic sinusitis, nasal obstruction, facial pain or other conditions.
Aetiological agents
Aspergillus fumigates is the most frequently isolated organism. These moulds are ubiquitous in the
environment. Less commonly A.flavus, S.apiospermum& Alternaria speices have been incriminated.
Epidemiology
Older individuals are appear to be more suspectible. No case have been reported in children. The
incidence of allergic rhinitis is no higher than in the general population.
Clinical features
Affected persons often present with long-standing symptoms of nasal obstruction, purulent nasal
discharge, cacosmia(fetid smell) or facial pain. The symptoms are often unilateral. Maxillary sinus is
most commonly involved, with partial or complete opacification, bone thickening & sclerosis;
occasionally bone destruction can occur. The sphenoid sinus is second most common site of
involvement.
Diagnosis
CT scans should reveal partial or total opacification of the involved sinus, often associated with
flocculent calcifications.
Histopathological investigation reveal material composed of a dense matted conglomeration of
fungal hyphae, separate from but adjacent to the mucosa of the sinus. No evidence of allergic mucin
in the sinus or granulomatous reaction in the mucosa. There should be no fungal invasion of the
mucosa, associated blood vessels or bone.

4. Management
Surgical removal of the fungus ball is the treatment of choice. No local or systemic antifungal
medication is needed.
Outcome & complications
Recurrence is rare but has been described as late as two years following the endoscopic removal of a
paranasal fungal ball. Patients who become immunocompromised are at risk of developing an
invasive fungal sinusitis.
Allergic fungal sinusitis
Definition : allergic fungal sinusitis is a non invasive disorder, seen in immunocompetent individuals,
which is increasingly being recognised as a cause of chronic rhinosinusitis. This disorder range from 5
to 10% of patients with chronic rhinosinusitis.
The diagnostic criteria of this condition are following: the presence in patients with chronic
rhinosinusitis (confirmed by CT), allergic mucin containing clusters of eosinophils& byproducts,
fungal hyphae on staining or culture.
Most experts also require the presence type 1 hypersensitivity to cultured fungi & nasal polyposis.
The diagnosis of allergic fungal sinusitis should not, however, be established or eliminated, on the
basis of results of the fungal cultures because of the vriable yield of these cultures.
The term eosinophilic mucin rhinosinusitis has been proposed to describe those patients with
chronic rhinosinusitis & allergic mucin in whom no fungal elements can be detected. It represent a
heterogenous group of pathophysiology mechanism all associated with eosinophilia, but in which
the predominant mechanism is a systemic dysregulation of immunological control.
It has been suggested that allergic fungal sinusitis is an allergic response to fungi in predisposed
individual.
Aetiological agents
In earlier reports, Aspergillus species were believed to be predominant cause of allergic fungal
sinusitis. More recently it is due to various dematiaceous environmental moulds, including
Alternaria , Bipolaris,Cladosporium, Curvularia & Drechslera speices.
Epidemiology
This condition occurs in young immunocompetent adults with chronic relapsing rhinitis,
unresponsive to antibiotics, antihistamines or corticosteroids. Although patients do not have
underlying immunodeficiencies, 50-70% are atopic. There is no male or female predominance.
Laregest number are reported in warm humid areas of the southern America where disorder
accounts for about 7% of all sinus surgeries.
Clinical manifestations
Many patients with allergies fungal sinusitis have a history of chronic rhinosinusitis & have
undergone multiple operations prior to diagnosis.

5. Patients present with unilateral nasal polyposis & thick yellow-green nasal or sinus mucus. Nasal
polyposis may form an expansive mass that causes bone necrosis of the thin walls of the sinuses.
Diagnosis
The diagnosis of allergic fungal sinusitis requires the presence of chronic rhinosinusitis in an
otherwise immunocompetent individual.
Laboratory test for eosinophilia, total serum IgE, specific IgE aganist fungal antigens,positive skin
prick test to fungal antigens.
CT scanning to assess the extent of disease.
Microscopic examination of the allergic mucin(either at the time of surgical debridement for chronic
rhinosinusitis or endoscopic examination for drainage) to determine the presence of eosinophils &
fungal elements.
Histological examination of sinus tissue to rule out invasion.
Fungal cultures are used to identify the responsible fungus.
The criteria for diagnosis are
-characteristic allergic mucin
- clusters of eosinophils
-Charcot layden
-the presence of fungal hyphae
- the presence of type 1 hypersensitivity.
Management options
Surgical debridement to remove the polyps & allergic mucin. Adjunctive medical treatment is also
required because all fungal element can not be removed. Commonly medical treatment nasal
corticosteroids, antihistamine, antileukotrienes sinonasal saline lavage & specific allergen
immunotherapy. Systemic antifungal treatment is ineffective on its.
Outcomes & complications
Postoperative endoscopic follow up is recommended because there is poor correlation between
subjective improvement & presence of objective regression of disease.
Despite surgical debridement & corticosteroid treatment, the condition may recurs upto 2/3rd of the
patients.

6. Candidiasis
The term candidiasis is used to refer to infections caused by organisms belonging to the genus
Candida. These opportunistic pathogens can cause acute or chronic deep seated infection, but more
often seen causing mucosal, cutaneous or nail infection. Oropharyngeal candidiasis is a commom
problem in debilited or immunocompromised persons. Isolated largyngeal candidiasis can also occur
in these individuals, but is much less common.
Epidemiology
Candidia albicans is present as a commonsal in the mouth of the adult populations. The number of
organisms in the saliva of carriers increases with tobacco smoking & dentures are worn.
Predisposing factors : debilitated patients such as those reciveing broad-spectrum antibiotic or
corticosteroids, DM, severe nutritional deficiencies, immunosuppressive disease(AIDS).
Local factors: unhygienic or ill-fitting dentures, tobacco smoking.
Prior to the introduction of combination antiretroviral treatment, oropharyngeal candidiasis was the
most common opportunistic infection seen in patients with HIV infection.
Clinical manifestations
Oral candidiasis can be classified into a number of distinct clinical forms.
-pseudomembranous candidiasis;
-erythematous (atrophic) candidiasis;
-hyperplastic( candida leukoplakia) candidiasis.
1) Pseudomembranous candidiasis is an acute infection, but can occur steroid inhalers,
immunocompromised individuals. It can also seen in neonates & terminally ill patients(leukaemia/
malignancies.), HIV patient. The lesion is painless although mucosal erosion or ulceration can occur.
The infection may spread to involve the throat, giving rise to severe dysphagia. The simple test is to
determine whether the pseudomembrane can be dislodged. If it can be wiped off to reveal an
eroded, erythematous & sometimes bleeding base, then this is diagnostic for pseudomembranous
candidiasis.
2) Erythematous candidiasis(atrophic candidiasis): is often associated with broad-spectrum
antibiotic treatment, chronic corticosteroid use& HIV infection or persistent pseudomembranous
candidiasis.
It can affect any part of the oral mucosa & manifests as a flat, red lesion, usually on the palate or
dorsum of the tongue. Lesion on the tongue present as depapillated areas.
3)Hyperplastic candidiasis(candidia leukoplakia): the lesion can undergo malignant transformation.
The lesion range from small palpable, translucent white areas to large dense opaque plaque, hard
rough on palpation. These lesion can not be removed. The lesion usually occur on the inside surface
of one or both checks, less commonly on the tongue. They are usually asymptomatic. Lesion that

7. contains both red erythroplakic & white leukoplakic areas must be regarded with great suspicion as
malignant change is often present.
4) chronic atrophic candidiasis or denture stomatitis: chronic mucosal erythema is associated with
oral prostheses.
Diagnosis
The clinical manifestation of oropharyngeal candidiasis are often characteristic, but can be confused
with other disorders. The diagnosis should be confirmed by microscopic examination & cultures.
Management
In infant pseudomembranous candidiasis can be treated with nystatin oral suspension
(100000units/ml) or amphotericin B oral suspension(100ml/ml). These should be dropped into
mouth after each feed or at 4 to 6 hours intervals. In most cases, the lesions will clear within two
weeks.(oral amphotericin B is not absorbed through the gut).
Older children & adults with nystatin/ amphotericin B oral suspension ( 1ml at six hour interval for
2/3 weeks). Or miconazole oral gel (250mg at six hour intervals). Treatment should be continued for
at least 48hours after all lesions have cleared & symptoms have disappeared.
Oral fluconazole (100-200mg/day) for 7 to 14 days than itraconazole & ketoconazole. Refactory
candidiasis can be managed with parenteral amphotericinB(.3-.5mg/kg per day for one week or
caspofungin(50mg/day)
The treatment of choice for laryngeal candidiasis is perenteral amphotericin B(.7-1mg/kg per day).
Airway obstruction managed by endotracheal intubation.
To reduce the likelihood of resistance developing, long-term azole treatment should be avoided
unless relapse is frequent or disabling.
The patient unresponsive to azole treatment can be managed with amphotericin B or
caspofungin.