rhinitis & rhino-sinusitis - alexu.edu.eg
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Zeyad MANDOUR- M.D; Ph.D.; A.F.S.A.Professor of O.R.L.Rhinology UnitORL department,Alexandria University
Rhinitis &Rhino-sinusitis
Rhinitis
Rhinosinusitis
Definition
As the lining of the nose and paranasalsinuses is continuous, inflammatoryprocesses tend to involve both areas.
Sinusitis
Defence- Mechanisms
1. Mucociliary system, √2. Epithelial integrity,3. Reflexes (cough, sneeze),4. Lysoszymes, opsonins &complement,5. Immnoglobulins (secetory IgA,
IgE)6. Macrophages & lymphocytes.
Mucociliary clearance:This depends upon
1.Amount of mucus.
2.Mucosal resorption
3.Patency of air current
4.Ciliary action.
Air current & Mucociliary clearance
safe
unsafe
unsafe
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Allergic Rhinitis
• Allergic rhinitis is an Ig.E mediatedhypersensitivity of nasal mucous membranecharacterized by:
• Sneezing, itching, watery rhinorrhea and asensation of nasal obstruction.
• It may also involve the lining of paranasalsinuses.
• It occurs in atopic individuals who are exposed tocommon aero-allergens
• It is genetically inherited either:Autosomal recessive.Autosomal dominant.
DefinitionDefinition
Allergens:
Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced rhinitis Role of pollution
Grass Pollen
Allergens:
Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced
rhinitis Role of pollution
House dust mites
Allergens:
Seasonal rhinitis Perennial allergic
rhinitis Occupational
allergens Food and drug
induced rhinitis Role of pollution
Domestic animals
Allergens:
Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced
rhinitis Role of pollution
Allergens:
Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced rhinitis Role of pollution
Allergens:
Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced
rhinitis Role of pollution
Intermittent Persistent
Mild Moderate toSevere
Classification
Intermittent
< 4 days/week Or< 4 days/week Or < 4 weeksconsecutive< 4 weeks
consecutive
Persistent
> 4 days/week & > 4 weeks
consecutive
Mild
Normal sleep
No impairment of daily activities
No troublesome Symptoms inuntreated patients
Moderate to Severe
Abnormal Sleep
Impairment of daily activity
Abnormal work
The Allergic reaction
Sensitization
Ig E Production
Arming of mast cells
Release of mediators
Clinical effects
IL-3, IL-5GM-CSF
Allergic rhinitis (mechanisms)
Allergen
Mast cell HistamineLeukotrienes
ProstaglandinsBradykinin, PAF
T lymphocytes(mast cells)
Immediate rhinitis symptomsSneezingItching
Watery dischargeNasal congestion
B lymphocytes
Ig E
IL-4
Eosinophilrecruitment
VCAM-1
Delayed ongoing rhinitisNasal blockageLoss of smell
Nasal hyper-reactivity
AR & Co-morbidities
Nasalpolyposis
AR & Co-morbidities
Clinical PicturePerennial
allergic rhinitisSeasonal
allergic rhinitis+
Mucoid + PND
+++
+++
++++
Watery
+
+
• Sneezing &Itching• Rhinorrhea
• Loss of tasteand smell• AssociatedsinusitisandEustachianDysfunction
Positive personal and family history of other atopic diseases
External signs
Allergic salute.
Mouth breathing.
Allergic shiners.
Pale bluish edematousnasal turbinates.
Polyps, septal deflection orprominent nasal turbinates.
Intranasal signs
Complications
Otitis mediaSinusitis
Allergic rhinitis and bronchial asthmafrequently coexist.
• Aspiration of secretions.• Dryness of LRT.• Increase vagal stimulation.• Bacterial toxins.• Inflammatory cytokines.
Therefore, treatment of rhinitis with improvement in nasal airwaymay also improve symptoms of bronchial asthma.
Investigations
Skin allergy test
An allergen extract is placedinto skin by either scratching
or pricking with a sharpdevice or by intradermal
injection using a syringe &needle.
Investigations
Blood test:
• Total IgE.
• Specific IgE (RAST test)
About 50% of patients with allergic rhinitis have normal levels oftotal IgE and 20% of non-affected individuals can have elevated
total IgE levels.
Investigations
Eosinophils:
Blood sample
Nasal smear
Only supports the diagnosis of allergicneither sensitive orrhinitis but it is
specific.
Non-allergic eosinophilic rhinitis.
Parasitic infection.
Management of Allergic Rhinitis
•Allergen Avoidance
•Pharmacotherapy
•Immunotherapy
Drug and Symptom MatrixDrugs and Symptoms Sneezing Itching Rhinorrhea CongestionAntihistamines ***** **** ***Anticholinergics(Ipratropium bromide) *****Corticosteroids ***** ***** *** ***Decongestants *****Mast Cell Stabilisers ***** *** *Antileukotrines *** ** ****
Adjunctive management1.Antibiotics
2.Mucolytic
3.Anti- leukotrienes
4.Irrigations- Saline douches
5.GERD control
6.FESS
7.Myringotomy +/- Grommettube insertion
Infective Rhinosinusitis
Infective Rhino-sinusitis-Non-specific or specificClassification• Acute Rhino-sinusitis• Chronic Rhino-sinusitis• Sub acute Rhino-sinusitis• Recurrent ARS• Acute Rhino-sinusitis superimposed on
CRS
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Infective viral RhinosinusitisAcuteCommon coldInfluenza
Common Cold
Rhinovirus Coronavirus
The commenst viral infection in human
Mode of Transmission
Predisposing factors
Cold weather. High humidity. Immune deficiency. Nutritional & Vitamin deficiency. Fatigue & stress. Nasal obstruction. Foci of chronic infection. General disease.
Viral Invasion
Release of mediators from infected cellse.g. IL-8, kinins, prostaglandins
Vasodilatation.Increase permeability.
Increase glandular secretion.Stimulation of parasympathetic
nerve endings.
Viral Invasion
Release of mediators from infected cellse.g. IL-8, kinins, prostaglandins
Clinical Picture
Clinical picture:• Fever, headache,malaise.• Dryness of nose.• Sore throat.• Sneezing.• Nasal obstruction.• Watery rhinorrhea.• MucopurulentRhinorrhea.• Resolution within5-10 days.
Complications:• Sinusitis.• Pharyngitis.• Adenoiditis.• Tonsillitis.• Otitis media.• Laryngotrachitis.• Bronchitis.• Pneumonia.• Nephritis.• Rheumatic fever.
Treatment: Bed rest. Vitamins. Fluids. Analgesic. Antipyretics. Antihistaminics. Anticholenergic. Decongestant. Antibiotics.
Influenza
One of the most common infectious diseases in human.
It is caused by influenza virusthat is classified as type A, B & C.
InfluenzaIt may occur in epidemics.
Spanish flu epidemic 1918 killed 20 millions all over the world.
InfluenzaTwo types of influenza virus.
Human influenzaAvian influenza
InfluenzaTwo types of influenza virus.
Human influenzaA person infected with a particular flu virusstrain develops antibody against that virus.
As newer virus strains appear throughantigenic shift and drift , the antibodiesagainst the older strains no longer recognizethe "newer" virus, and infection with a newstrain can occur.
Common Uncommon
PneumoniaOtitis media Tracheobronchitis
Acute sinusitis
Reye's syndromePericarditis
MyositisMyoglobinuria Encephalitis
Transverse myelitisGuillain-Barré syndrome
Rhabdomyolysis
Complications
• Healthy children six to 23months of age.• Adults 65 years and older.• Persons six months to 64 yearswith cardiopulmonary, respiratory,renal, metabolic, orimmunodeficient conditions.• Pregnant women
Features Influenza Common cold
Onset Abrupt More gradualFever Common up to 40.0°C Uncommon only 0.5°C
Myalgia Severe, common UncommonArthralgia Severe, common UncommonAnorexia Common UncommonHeadache Severe, common Severe, common
Cough (dry) Common, severe Mild to moderateMalaise Severe Mild
Fatigue, weakness More common Very mild, short lastingChest discomfort Common, severe Mild to moderate
Stuffy nose Occasional CommonSneezing Occasional Common
Sore throat Occasional Common
1. Children aged 6–23 months.2. Adults aged ≥50 years.3. Persons aged 2–64 years with underlying
chronic medical conditions.4. Women who will be pregnant during the
influenza season.5. Residents of nursing homes and long-term
care facilities.6. Children aged 2–18 years on chronic
aspirin therapy.7. Health-care workers involved in direct
patient care; and8. Out-of-home caregivers and household
contacts of children aged <6 months.
Vaccination
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Infective bacterial Rhinosinusitis
Chronic non-specific• Simple chronic rhinitis• Chronic hypertrophic rhinitis• Chronic atrophic rhinitis
1. Simple chronic rhinitis• Repeated attacks of acute rhinitis• Maintenance of acute
inflammatory condition by one ormore of the following factors:
1. Neighboring infection (sinusitis,tonsillitis or adenoiditis)
2. Chronic nasal obstruction(deviated septum or vasomotorrhinitis)
3. Ciliary stasis (ciliarydyskinesia))
Simple chronicrhinitis4. Chronic irritation (smoke,
tobacco, dust orvasoconstrictor abuse )
5. Metabolic imbalance (dietimbalance, excessivecarbohydrate, gout orvitamins deficiency)
6. Endocrine factors (diabetes,thyroid)
Simple chronic rhinitis- clinicalfeatures• Nasal obstruction (chronic
hyperaemia, nasopulmonary reflex)• Post nasal discharge• Headache• Transient anosmia
Simple chronic rhinitis-Examination
• Red mucosa (active infection)• Purple mucosa (venous stasis)• Other areas (pal and edematous)• Mucous strands
Simple chronic rhinitis-Management• Correcting predisposing factors• Nasal wash• Topical +/_ systemic steroids• ABCS +/_
2. Chronic hypertrophicrhinitis
• Advanced stage of non specificchronic with permanent wholemucosa hypertrophy
• Thick, nodular mucosa especiallyat the posterior end of the inferiorturbinate (mulberry like)
• Sometimes polyps may form• +/_ Rhinitis medicamentosa
Chronic hypertrophicrhinitis
• Same os simple chronic rhinitis• +/_ surgical trimming• +/_ out fracture
Chronic nasal disease characterized by progressive atrophy ofnasal mucosa and the underlying bone of the turbinates withformation of scanty viscid secretions that rapidly dries toform crusts that emit a characteristic foul odor (ozaena).There is associated abnormal patency of nasal passages.
3. Atrophic rhinitis
The exact cause is unknown1) Chronic bacterial infection; Klebsiela, Pertussis,
Diphtheria.
2) Nutritional Deficiency; Vit-A deficiency, Fedeficiency.
3) Endocrinal Factor; estrogenic deficiency.
4) Autoimmune.
Etiology (primary)
Incidence
• Endemic in subtropical & temperate climates.
• In Egypt, it affects 1% of the population.
• More in those living in unhygienic conditions.
• It occurs more commonly in females at the time of
puberty and this supports the hormonal theory of
the role of estrogen in the etiology of atrophic
rhinitis.
Etiology
Chronic bacterial infection: Coccobacillus. Bacillus pertussis or
mucosus. Klebsiella ozaenae. Diphtheroid bacilli.
Etiology
Nutritional Deficiency:
▫ Vitamin A deficiency.▫ Iron deficiency.
Etiology
Autoimmune Disease:Due to loss of tolerance
• Viral infection.• Malnutrition.• Immunodeficiency.
Etiology
Endocrinal factorMainly estrogen deficiency; the proof is:
Occurrence in girls around puberty. Aggravation of symptoms during menstruation. Improvement of some cases by estrogen therapy.
Etiology (secondary)
1. Excessive surgicaldestruction of nasal mucosa.
2. Chronic exposure to irritant,cocaine or toxic agents
3. Healed stage ofgranulomatous disease.T.B., Scleroma.
4. Radiotherapy.
Endarteritis & Periarteritis
Atrophy of mucosal & submcosal structures
Decrease nasal secretions Abnormal nasal patency
Dryness of secretions & crust formation
Histopathology
• Sub epithelial cellular infiltration (Accumulation of chronic inflammatory cells e.g.lymphocytes and plasma cells).• Ciliary destruction. )•Atrophy of the boney turbinates ( Decrease insize of mucosal & submucosal structures) and(Decrease in number and size of compoundalveolar glands).• Metaplasia from ciliated columnar to squamousepithelium.•Endarteritis obliteransIn Type I : Endarteritis obliteransIn Type II: Dilated capillaries.
Clinical Picture
Symptoms Signs
•Nasal obstruction.•Headache.•Epistaxis.•Bad odor from thenose.•Pharyngitis sicca.•Chocking.
• Fetor oris.• Green, yellow or blackcrusts.• Ulcerated bleedingmucosa.• Atrophy of inferior &middle turbinates.
Characteristic CT findings
Mucosal thickening of the paranasalsinuses.
Loss of definition of the ostiomeatalcomplex secondary to resorption of
the ethmoid bulla ad uncinateprocess.
Hypoplasia of the maxillary sinuses.
Enlargement of the nasal cavitieswith erosion and bowing of the
lateral nasal wall.
Bony resorption and mucosal atrophyof the inferior and middle turbinates.
Conservative measuresNasal cleaning; Regular nasal cleaning , lubricant
oil drops, glucose and glycerin.2) Vit E and iron supplement3) Hormonal therapy.4) Corticosteroids.5) Vasodilators.6) Antibiotics
Treatment
Surgical techniques---1Cavity narrowing techniques:Nasal closure1) Complete closure; Skin flaps.2) Partial closure; 3 mm hole.3) Post choana closure.Aim: decrease dryness, crustation.
Nasal Implants1) Auto grafts; cartilage.2) Autogenous osteoperiosteal flaps.3) Submucosa Teflon4) Synthetic implants as silicon
Surgical techniques---2
PharyngoplastyCaudally based pharyngeal flaps.
Cavity moistening techniques
1) Salivary irrigation procedures.2) Dennervation procedures.
Surgical techniques---3
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Infective bacterial RhinosinusitisChronic specific• Syphilis• T.B• Rhinoscleroma
1. Syphilis• May be encountered in
primary, secondary, tertiary orcongenital forms (snufflespurulent rhinitis)
• Mucous membrane ulcerationand discharge occur incongenital and secondarysyphilis
Syphilis• Gummas of the tertiary stage give rise to
septal perforations (bone and cartilage)
• Destroy the surrounding nasal skeleton
with a shrunken bridge deformity
• DX : clinical features and Treponema
Pallidium identification in smears from
primary and secondary lesions
• Also by serological tests in tertiary stage
2. Tuberculosis• Rare complication of pulmonary TB• Ranging from ulcerative,
hypertrophic (tuberculoma) andfibrotic types
• Fibrotic often affects surroundingfacial skin (lupus)
• Cartilaginous septum Tuberculomamay lead to ulceration andperforation (no bone involvement)
• Biopsy is diagnostic and treatmentsimilar to lung condition
3. Scleroma• Chronic specific infection of the respiratory tract
esp. the nose (rhinoscleroma)• Klebsiella rhinoscleromatis• Mode of infection (unknown)• Not uncommon in Egypt• Teenagers especially in females (poor classes)• Granulomatous tissue infiltrates the submucosa
of the nose with accumulation of chronicinflammatory cells (plasma cells, lymphocytesand fibroblasts)
Scleroma• Spread to involve (nose, nasopharynx,
oropharynx) with soft palate fibrosis,subglottic stenosis and rarely trachealand bronchial, maxillary sinus andmiddle ear or ET or lacrimal sacinvolvement
Hebra nose
Scleroma- pathology• The infiltration is charecterized by
the presence of:• Miculicz cells (large foam cells
containing the causative bacilliwithin its vacuoles)
• Russel bodies (degeneratedplasma cells with an eosinophilstaining cytoplasm)
Scleroma- pathology
• Electron microscopy showsanother
type of cells called Mott cellswhich are
(plasma cells containinginclusion bodies)
They are intermediate stage b/wplasma cells and Russel bodies
Scleroma- clinical features• Catarrhal• Hypertrophic: overgrowth of
dense fibrous tissue• Atrophic : process of
reabsorption and breakdownof tissues
• Cicatricial: scar left by theformation of new connectivetissue over a healing sore orwound.
Scleroma- pathological features
• Hypertrophic: overgrowth ofdense fibrous tissue
• Atrophic : process ofreabsorption and breakdownof tissues
• Cicatricial: scar left by theformation of new connectivetissue over a healing sore orwound.
Scleroma- management• The organism can nevertheless be extremely difficult to
be eradicated by antimicrobials.• Once the diagnosis has been confirmed by biopsy,
treatment must be intense and prolonged.• Bactericidal antibiotics in large doses are given in large
doses for a minimum of four to six weeks and arecontinued until two consecutive cultures from biopsymaterial are proven negative.
• Initial surgical debridement prior to chemotherapy is reportedto be useful in granulomatous stage.
• The traditional antibiotics used are streptomycin andtetracycline, but the lenghthly nature o the treatment can leadto problems with adverse effects and compliance.
• Recent reports have emphasized the good results achieved withoral therapy with rifampicin, sulphamethoxazole- trimethoprimcombination, and ciprofloxacin.
• Local application of 2 percent acriflavin for a period of eightweeks has been noted to be both efficacious and non-toxic.
• Locally applied rifampicin has been used with success.
Scleroma- management
• Radiation to total dose of 3000 - 3500 Gy over three weeksdestroys scleroma but, the currently available antimicrobials, isunlikely to be required.
• In late cases where disease has been eradicated, further plasticreconstructive surgery may be required.
• This may be carried out by nasal endoscopy and laser, ifappropriate.
Scleroma- management
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Granulomatous Rhinosinusitis• Sacoidosis• Wegener’s granuloma• Midline leathal granuloma (Stewart’s
granuloma)
1. Sarcoidosis• Idiopathic systemic
granulomatous disease• Frequent head and neck
manifestations• In the nose, the mucosa
becomes swollen and granular• Crusting and stenosis• +/_ neck adenopathy, hilar
adenopathy, eye and boneproblems
Sarcoidosis• Biopsy from nasal septum or
turbinates is often diagnostic
• Topical steroid sprays are
useful to control symptoms
2. Wegener’s granuloma• Autoimmune collagen
disorgers with multisysteminvolvement
• The respiratory tract, kidneysand skin are the most ofteninvolved
• Charecterized by a necrotizingvasculitis
• Ulceration of the septum withcrusting and saddle nose arecommon nasal presentations
Wegener’s granuloma• Biopsy id diagnostic• ESR is raised• Microscopic haematuria and
proteinuria• Can be controlled for many
years with steroids andcyclophosphamide
3. Midline lethal granuloma(Stewart’s granuloma)
• A rare locally destructive lesion• Radiotherapy and
chemotherapy may halt theprocess
• Most cases progress rapidly todeath
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Non-allergic, non-infectiverhinosinusitis1. NARES2. Vasomotor rhinitis3. Rhinitis medicamentosa4. Chronic atrophic rhinitis5. Chronic hypertrophic rhinitis
Non-allergic, non-infective-ClassificationI. (NARES) (Jacobs, 1987) is characterized by the
presence of nasal eosinophilia in subjects whoare often middle-aged and who have perennialsymptoms of sneezing paroxysms, nasalitching, rhinorrhoea and occasionally loss ofsense of smell.
• However, they lack evidence of allergic diseaseas determined by skin tests and IgE levels.
Non-allergic, non-infective-ClassificationII. Vasomotor rhinitis
III. Rhinitis medicamentosa
IV. Chronic atrophic rhinitis √√
V. Chronic hypertrophic rhinitis √√
Rhinosinusitis
Allergic Infective viral& bacterial
Non allergicnon infective
Acute Chronic
Nonspecific
Chronicsimplerhinitis
SpecificCommon coldInfluenza
Atrophicrhinitis Syphilis
T.B.Scleroma
Granulomatous
SarcoidosisWegenerStewart
NARESVasomotor rhinitis
Rhinitismedicamentosa
Hypertrophicrhinitis
Infectivefungal
Infective fungal rhinosinusitis1. Invasive2. Non-invasive
Fungal Sinusitis• Invasive
▫ Presence of fungal hyphae within the mucosa,submucosa, bone, or blood vessels of theparanasal sinuses
• Non-invasive▫ Absence of fungal hyphae within the mucosa and
other structures of the paranasal sinuses
Fungal Sinusitis - Classification• Invasive
1. Acute Invasive Fungal Sinusitis2. Chronic Invasive Fungal Sinusitis3. Chronic Granulomatous Invasive Fungal Sinusitis
• Non-invasive1. Allergic Fungal Sinusitis2. Fungus Ball (fungus mycetoma)
1. Acute Invasive Fungal Sinusitis• Most lethal form of fungal sinusitis – mortality
50-80%• Rare in immunocompetent patients• Two clinical populations
▫ Poorly controlled Diabetics – ususally caused byfungi of order Zymocycetes (Rhizopus, Rhizomucor,Absidia, and Mucor)
▫ Immunocompromised with severeneutropenia (chemotheraphy patients, BMT, organtransplants, AIDS) – Aspergillus accounts for 80% ofinfection in this group
2. Chronic Invasive FungalSinusitis
• Usually immunocompetent• History of chronic rhinosinusitis• Usually persistent and recurrent disease• Maxillofacial soft tissue swelling, orbital
invasion with proptosis, cranial neuropathies,decreased vision, can invade cribiform platecausing headaches, seizures, decreased mentalstatus
3. Chronic GranulomatousInvasive Fungal Sinusitis
• Primary paranasal granuloma and indolentfungal sinusitis
• Primarily found in Africa (Sudan) and SoutheastAsia, only few case reports in US
• Immunocompetent• Caused by Aspergillus flavus• Characterized by non-caseating
granulomas in the tissues
4. Allergic Fungal Sinusitis
• Most common form of fungal sinusitis• Common in warm, humid climates of
Southern US• Hypersensitivity reaction to inhaled
fungal organisms resulting in chronicnoninfectious inflammatory reaction - IgEtype I immediate hypersensitivity and type IIIhypersensitivity are involved
• Common organisms implicated – Bipolaris,Curvularia, Alternaria, Aspergillus, andFusarium
Allergic Fungal Sinusitis – Clinical-cont.• “Allergic mucin” within affected sinus
which is inspissated mucous theconsistency of peanut butter witheosinophils on histology
• Younger individuals, third decade,immunocompetent
• Often associated history of atopy withallergic rhinitis or asthma
• Chronic headaches, nasal congestion, andchronic sinusitis for years
5. Fungus Ball
• Older individuals, female>male• Immunocompetent• Asymptomatic or minimal symptoms with
chronic pressure or nasal discharge• Cacosmia (perception of foul odor when no
such odor exists)
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