7. Catarrhal Stage: prolonged purulent rhinorrhea,
crusting, and nasal obstruction
Nodular/granulation stage: to local destruction
and cosmetic deformity.
Broadening of the nasal dorsum produces the
characteristic Hebra nose
9. Cicatrizing stage: Nasal or nasopharyngeal
stenosis is common.
Stenosis of the larynx or trachea can cause life-
threatening airway obstruction.
10. Granulomatous tissue characterized by:
Mikulicz (foam) cells: macrophages with
vacuolated cytoplasm, central nucleus &
phagosomes containing Frisch bacilli
Slime layer
nondigestible mucopolysaccharide in the
phagosomes of macrophages
11. Russel (Hyaline) body:
eosinophilic structures within the cytoplasm of
plasma cells
Treatment:
Usually self limiting
13. History:
1892 - Malbran observed the organism in nasal
polyp
1900 - Seeber described the organism
1905 - Minchin & Fantham studied O'Kineley's
tissue and named the organism as
Rhinosporidium Kinealyi
1936 - Cefferi establised the identity of R.
Seeberi and R. Equi
1953 - Demellow described the mode of its
transmission
14. Chronic granulomatous infection of the mucous
membrane by Rhinosporidium seeberi, mainly
affecting nose & nasopharynx
Caused by – R. seeberi
Seen in India ,Pakistan, Sri Lanka
15. Theories of mode of spread:
Demellow's theory of direct transmission
Autoinoculation theory of Karunarathnae
(responsible for satellite lesions)
Haematogenous spread - to distant sites
Lymphatic spread - causing lymphadenitis
16. Mature sporangium –
100 - 400 microns in diameter, with a thin
bilamellar cell wall.
Inside the cytoplasm immature and mature
spores are present.
Electron dense bodies are seen in the
cytoplasm.
The bilamellar cell wall has one weak spot
known as the operculum.
The mature spores find their way out through
this operculum on rupture.
Mature spores give rise to electron dense
bodies which is infective unit.
17. Epistaxis ,nasal discharge, nose block
Nasal mass: papillomatous or polypoid, granular,
friable, bleeds on touch, pedunculated or sessile,
pink surface studded with white dots [Strawberry
appearance], involves septum & turbinates
18.
19.
20. Dapsone: arrest the maturation of the sporangia
and promote fibrosis in the stroma
Surgery:
Total excision of the polyp, preferably by electro-
cautery.
Pedunculated polyps permit of radical removal
Sessile polyps with broad bases-recurrence
21. Aspergillus is a common saprophyte of soil
and decaying organic material such as fruit
filamentous fungus that has septate hyphae
and reproduces as asexual conidia.
Aspergillus fumigatus, A flavus, and A Niger.
Aspergillus is recognised by the septate
hyphae and dichotomous branching at an
angle of 45°
22.
23. A. Flavus :more indolent, chronic invasive fungal
disease seen primarily in the Sudan and in
India, but it can also be responsible for fulminant
invasive disease regardless of geographic
location.
Aspergillus species can be angioinvasive, but
they do not cause the obliterative invasion seen
with mucormycosis.
24. Fulminant aspergillosis :
The clinical findings:
Prominent non-tender facial cutaneous
erythema and oedema may be an early
manifestation.
Ulceration of the nasal mucosa and destruction
of the inferior turbinates may be seen.
The infection will progress with destruction of
the sinuses, angio-invasion, and extension into
the orbit and brain.
Little tissue reaction and no granulomatous
response is seen
25. Invasive aspergillosis: presents clinically as an
enlarging mass in the cheek, orbit, nose and
paranasal sinuses region.
Proptosis is often a prominent feature.
There is a granulomatous response to
Aspergillus hyphae with considerable fibrosis.
The inflammatory process extends beyond the
bony walls of the sinuses into the soft tissues of
the cheek and orbit. Extension into the brain can
occur
26. Management:
systemic antifungal treatment such as
amphotericin B
surgery is usually required for invasive
asperigillosis and sometimes with the fulminant
form.
27. Three hypotheses:
1)A prokaryote cyanobacterium in the genus
Microcystis is the etiologic agent of
rhinosporidiosis
2)R. seeberi is a eukaryote pathogen in the
Mesomycetozoa
3) R. seeberi is a fungus
Further studies are needed to validate R.
seeberi's acquisition of prokaryote plastids and
other issues that still need careful scrutiny
28. Introduction
Active ketone reductase system (Rhizopus)
Hyperglycemia: fungal growth and impairs
neutrophil chemotaxis
Iron-rich environment
29. Pterygopalatine fossa
Spread
Thrombosis in the cavernous sinus, carotid
arteries, and jugular vein.
70% in Diabetes Mellitus
30. Acute invasive fungal sinusitis
Unilateral nasal discharge and black crusts due to
ischaemic necrosis
Proptosis, ophthalmoplegia
Fibrosis & granuloma formation seen in chronic
invasive fungal sinusitis
Locally destructive with minimal bone erosion
37. Primary acquired syphilis
Primary chancre: Genital
• Hard, nonpainful, ulcerated papule with enlarged
Rubbery Lymph nodes
• Self limiting
• Disappears in 6 to 10 weeks
38. Secondary acquired syphilis
• 6 to 10 weeks after inoculation
• Simple catarrhal rhinitis
• May be crusting and fissuring of nasal vestibule
• Rarely recognized in nose
• Secondary syphilis is a period of spirochetemia
• Serological tests
• Scar of primary lesions
39. Tertiary syphilis:
• 1/3 rd of secondary syphilis progress to tertiary
syphilis
• After 2 years of inoculation
• Gumma: begins as subcutaneous nodule
• Bony portion of septum most commonly
involved
• Rarely lateral nasal wall, frontal sinus, nasal bones
40.
41. • Morbidity & Mortality: Late manifestations in
skin, bones, CNS and viscera(heart and Great
vessels)
Diagnosis:
VDRL
Biopsy
TPHA
FTA-ABS
42. Benzathine penicillin 2.4 million units i.m weekly
x 3week
Copious alkaline douches
Yellow mercury oxide ointment
43. 1. Vestibular stenosis
2. Perforation of nasal septum
3. Secondary atrophic rhinitis
4. Saddle nose deformity
44. Causative organism and spread
Three forms:
1. Lupus vulgaris (Nodular form)
2. Ulcerative Form
3. Sinus granuloma
45. Low grade tubercular infection
Nasal vestibule, skin and mucosa
Direct inoculation
Apple-jelly nodules
Blanching maneouvres
Progressive scarring and deformity
46.
47. Malignant transformation of scar is seen
Ulcerative Form
Cartilaginous septum or inferior turbinate
Nasal obstruction, epistaxis, crusting or
discharge
Progress to septal perforation but dorsal
saddling does not occur.
Bony septum not involved
48. Diffuse soft tissue swelling and multiple discharging
sinuses in supraorbital region
CT and MRI
Orbit and nerve may be involved
50. Caused by Mycobacterium leprae
Dissemination via nasal secretions
Tuberculoid Leprosy:
• Strong host resistance
• Solitary, anaesthetic cutaneous lesions with
involvement of sensory or motor nerves.
• Skin of nasal vestibule can be involved
51. Lepromatous Leprosy:
• Diffuse infiltration of skin, nerves and mucosal
surfaces
• Nasal obstruction, crust formation and blood
stained discharge
• Late manifestations: Atrophic rhinitis, septal
perforation and dorsal saddling
• Hyposmia seen in 40% patients
52.
53.
54. Diagnosis:
Treatment:
Paucibacillary:
Dapsone 100mg OD, Rifampicin 600mg once a month
Multibacillary: Dapsone 100mg OD, Rifampicin 600mg
once a month and Clofazimine 300mg once a month and
50mg daily
Direct intranasal administration of rifampicin
Local Betnovate (one part) in unguentum(two parts)
55. Definition:
Granulomatous inflammation, involving the
respiratory tract and necrotizing vasculitis affecting
small- to medium-sized vessels
The pathological hallmark is the coexistence of
vasculitis and granulomas
56. Age and sex:
15 to 73 years
Halstead's series reports
Aetiology:
Unknown.
Hypersensitivity reaction with an immune response to
an unknown stimulus.
It has been postulated that this may be related to
inhaled bacteria
57. The deposition of the immune complexes is
thought to be responsible for vasculitis in other
conditions
Van der Woude in 1985 who found antibodies reacting
with the cytoplasm of ethanol-fixed granulocytes and
monocytes in patients with Wegener's granulomatosis
Two main forms of ANCA: pANCA and cANCA.
58. As late as the early 1970s, Wegener's granulomatosis
remained a serious and lethal disease.
Rapid diagnosis remains of great importance since a
fulminating course with a fatal outcome can occur in as
little as 48 hours.
Minor ENT symptoms
Destruction of the intranasal structures
Minor nasal surgery and/or repeated biopsies
62. RENAL
Both casts and red cells
Microscopic evaluation of a midstream specimen of
urine
Segmental or diffuse glomerulonephritis
63. OCULAR
Conjunctivitis, dacrocystocystitis, episcleritis and
corneal ulceration, but optic neuritis and retinal artery
occlusion can also occur.
Proptosis (20%) from a granulomatous mass within the
orbit or extending from the adjacent sinuses.
Blindness
64. ORAL
Hyperplastic granular lesion of the gingiva beginning in the
area of the interdental papillae
Extensive ulcerative stomatitis
LARYNGEAL AND TRACHEAL
Subglottis and upper trachea
laryngotracheal obstruction
Gentle dilation, internal stenting and localized steroid
injection
65. Diagnosis:
cANCA test: 95 percent of patients in generalized active disease
60 percent with localized disease
Urine analysis ,chest x-ray and other respiratory function tests
Extravascular foci of necrosis in lung biopsy samples has recently
received attention as a characteristic feature of WG
66. Imaging:
Computerized tomography and MRI:
mucosal thickening in the nasal cavity or paranasal sinuses
Bone destruction and new bone formation in the
walls of the sinus cavities
Imaging of the chest: cavitation followed by fibrosis
67. Treatment:
The report by Fahey et al.:
Steroids and a variety of cytotoxic drugs
Renal damage prior to commencing treatment is the
major prognostic factor
The ESR, CRP and c-ANCA test
68. Harrison's Experience:
Prednisolone (60-80 mg/day) with cyclophosphamide
(2 mg/kg) or azathioprine (200 mg/day) should
produce a dramatic improvement in acute disease
In Harrison and Lund's series, azathioprine with
prednisolone produced 100 percent immediate control
in 48 cases
69. Plasma exchange immunogloulin infusion,
methotrexate and cyclosporin
Bone densitometry and bisphosphonates
Nasal: intranasal steroids, glycerin drops and saline/
alkaline douching
70. Systemic condition of unknown aetiology
Young adults between the third and fifth decades
Sex: female preponderance of 2: 1
Incidence of sino-nasal sarcoidosis
71. Pathogenesis:
Process initiated by an antigen presenting cell,
probably an alveolar macrophage
Monocyte activation and granuloma formation
The persistence of the granuloma may be ascribed to
continued antigenic stimulation
72. Histology:
sarcoid granuloma is characterized by epithelioid cells
surrounded by lymphocytes and fibroblasts but devoid
of caseation
Crystalline or calcified inclusion bodies are sometimes
seen, e.g. Schaumann bodies
73.
74. Clinical features:
Uveo-parotid fever (Heerfordt’s disease)
Cutaneos sarcoidosis (Lupus pernio)
Otologic sarcoidosis
Lymphoid hyperplasia and adenoidal enlargement
Thoracic involvement either within the lung itself or
affecting intrathoracic lymph nodes
75.
76. Anosmia
Epiphora
Nasal septum and submucosal sarcoid
Soft tissue of the supraglottic larynx may become
thickened
77.
78.
79.
80. Diagnosis:
Kveim test
Angiotensin converting enzyme (ACE)
Imaging (chest x-ray, computerized tomography (CT)
perfusion studies
Bronchoalveolar lavage and gallium-67 scanning, are
generally performed combined with biopsy of
potentially affected tissue
81. Staging system by Krespi et al:
stage I: mild, reversible nasal disease without
paranasal sinus involvement
stage II: moderate disease, potentially reversible, with
paranasal sinus involvement
stage III: irreversible disease
82. Treatment
Limited disease undergo spontaneous remission
without specific treatment
Topical: intranasal steroids, either sprays or
drops, glycerine drops ,nasal douching and irrigation
Surgery generally is contraindicated in active
disease
83. Midline destructive granuloma or T/NK cell lymphoma
May occur at any age from the first to the ninth
decade, though the median is fifth or sixth decades
Male preponderance
Epstein barr virus
84. (WHO) classification:
1.Extranodal NK/T-cell lymphoma or nasal type
2.Aggressive NK cell leukemia
Polymorphic reticulosis
Lymphomatous infiltrate: angiodestruction, leading to
coagulative necrosis
Marrow hemophagocytosis may occur
85. Clinical features
three stages:
1. Prodromal: persistent nasal obstruction and rhinorrhoea
2. A period of activity:
Progressive destruction of the nasal framework, palate,
upper lip extending into the pharynx and orbit and skull
base
3. The terminal stage: Haemorrhage associated with the
gross mutilation of the face and exhaustion lead eventually
to death
86.
87.
88. Diagnosis:
Large biopsy material from tissue beneath the slough
and crust
Immunohistochemistry using a panel of monoclonal
antibodies against T-cell differentiation
EBV genomic fragments in plasma
89. Imaging
Dramatic and progressive destruction of the midline
soft tissue and bone without a gross tumour mass are
typical
Treatment
SMILE (dexamethasone, methotrexate, ifosfamide, L-
asparaginase, and etoposide)
90. LVP regimen (L-asparaginase, vincristine, and
prednisolone) for 6 courses, with sandwiched
radiotherapy after 2 courses
Radical full course radiotherapy of 55 Gy or more with
wide field coverage
92. Clinical features
Most patients are under 20 years of age and there is a
female to male preponderance of 2: 1
Pain and swelling over the affected
bone,diplopia,hearing loss,vertigo and tinnitus
Maxilla and mandible
93.
94. Diagnosis:
Serum calcium and alkaline phosphate
Imaging
The lesions are expansile and lytic with a 'soap
bubble’ , well-demarcated edges
96. Definition
Granulomatous reaction to cholesterol crystals
Age: 26 to 56 years
male preponderance
Maxilla or frontal sinuses producing expansion of the
bone and cosmetic deformity
97. Imaging
The lesion produces a cyst-like expansion of the bone
and or sinus
Histology
Typical appearance of granulation tissue containing
foreign body-type giant cells surrounding clefts created
by the cholesterol crystals
100. Clinical features
Age: 85% in first three decades
Whilst all organs may be affected, the skull is a
common site of involvement
Painful swelling of the involved bone
Involvement of the temporal bone may simulate acute
mastoiditis
101. Imaging
punched out bony lesions
Radiolucent areas around the teeth
Lesions in the skull often show bevelled margins due to
angulated destruction of the cortical bone
102. Histology:
Langerhans' cells are mixed with other inflammatory
cells
Intense osteoclastic activity at the periphery of the
granuloma
During the healing phase of the granuloma, the stroma
becomes increasingly fibrotic
Birbeck granules on electron microscopy
103.
104. Treatment:
Type I disease
Chemotherapy etoposide and steroids for 12 months
Alpha interferon and bone marrow transplantation
Type II disease:
Curettage/excision and radiotherapy
