This document discusses ear, nose and throat infections. It describes the anatomy and defenses of the ear canal, middle ear, and inner ear. It discusses common bacterial and fungal causes of otitis externa, otitis media, sinusitis, tonsillitis, and rhinoscleroma. Treatment options are provided for various ear, nose and throat infections. Rare infections like mucormycosis, fungal balls, and rhinosporidiosis are also mentioned.

1. Ear, Nose and
Throat infections
Dr. Ihsan Edan Alsaimary
Dept.Microbiology , College Of Medicine-
University Of Basrah , Basrah- Iraq
ihsanalsaimary@gmail.com

2. Ear canal
 Ear canal 2.5 cm sac.
 Cartilaginous covered
by layers of sebaceous
and apocrine glands
and hair.
 The glands produce a
thin layer of ceruman.

3. Defence mechanisms of ear
 Outer ear
 Hair
 Ceruman
 Internal ear
 External bony part of the labyrinth has
perilymph
 Internal membrane part contains endolymph

4. Antibacterial properties of ceruman
 Contains lysozyme.
 Contains saturated fatty
acids.
 Has a pH of 6.9
 Lateral epithelium
migration towards external
os mechanically cleans the
ear canal.
 Insufficient ceruman
predisposes to ear
infection.

5.  Perforation of tympanic
membrane due to
insertion of a 'q' tip. This
is likely to result in both
an otitis media and otitis
externa

6. Otitis externa
 Acute localised otitis externa
 Acute diffuse otitis externa
 Chronic otitis externa
 Malignant otitis externa

7. Ear swabs
 Culture of ear swabs
 Used for OE not very useful for OM
unless fluid from the middle ear is
swabbed
 Neonatal screening

8. Acute OE
 Majority of infections are due to
bacteria – Staphylococcus aureus,
Pseudomonas aeruginosa,
anaerobes
 Fungal infections account for only
10%

9. Acute OE
 Acute localised OE usually caused by
Staph.aureus which causes furuncles or
pustule of a hair follicle.
 Acute diffuse OE. Also called ‘swimmers
ear’ and is associated with hot humid
conditions. Polymicrobial infections usually
involving Staph.aureus, pseudomonas and
anaerobes.

10. Treatment of acute OE
 Usually using topical rather than systemic
antibiotics unless there is significant
infection of the pinna and surrounding
tissues.
 In less severe cases topical antibiotics and
steroid are all that is required. In more
severe cases suction of debris and
application of wicks or packs of antibiotic
and steroids are required.
 Aminoglycosides such as neomycin or

11. Chronic otitis externa
 External auditory canal with
Aspergillus overgrowth
manifesting as a cottony matrix
topped by small black balls.
 Chronic OE is usually
caused by colonization
by coliforms or fungi
and is best treated by
topical cleansing
rather than antibiotic
treatment.
 Rarely caused by
syphilis or leprosy

12. Malignant otitis externa
 Malignant external otitis with pus
draining from the necrotic ear canal
and underlying osteomyelitic bone.
 Life threatening condition
affecting diabetics, the
immunocompromised and
elderly.
 Severe necrotizing infection of
soft tissues, bones, blood
vessels and cartilage with risk
of neurological involvement
and facial paralysis.
 The patient requires hospital
admission and treatment with
high dose antibiotics, surgery
to debride dead tissue and
occasionally hyperbaric
treatment.

13. Non-bacterial cause of OE
Ramsey Hunt Syndrome –
Herpes Zoster Oticus. Severe
otalgia, facial paralysis and
varicelliform rash over the
pinna. Treated with antivirals.

14. Otitis media
 Occurs between the ear drum and the inner
ear and includes the eustachian tube.
 It is defined by the accumulation of fluid in
the middle ear with symptoms of acute
infection.
 Serous OM or Sterile OM does occur and is
often attributed to an allergy or radiation
treatment.

15. Acute Otitis media
 Usually caused by migration of bacteria from the
naso-pharynx up the eustachian tube and into the
ear.
 Common disease of children (80% - 90% by the
age of 2 years old) with frequent recurrence of
infection. The highest incidence rate is between 6-
24 months old.
 This is because up to the age of seven years the
eustachian tube is relatively short, and more
horizontal than in older children & adults.
 It is important to treat as it can lead to hearing loss
and affect the speech and behaviour of children.

16. Acute OM (pathogens)
 Often viral – RSV and parainfluenzae
 Can lead to bacterial infections usually due
to S.pneumoniae, H.influenzae and
Moraxella species.
 Less commonly S.pyogenes, S.aureus,
enterobactericaea and anaerobic Gram
negative non-sporing rods such as
Prevotella, Fusobacteria, Porphyromonas
and Bacteroides .

17. Chronic OM
 Caused by perforation of the tympanic membrane
or problems with immune function.
 Very destructive and persistent and can result in
loss of hearing. May be associated with
mastoiditis.
 Commonly caused by pseudomonades and
S.aureus including MRSA. Anaerobes and fungi
are found in a quarter of cases. More likely to be
polymicrobial than acute OM.
 Can be caused by viruses – RSV, Influenza,
enteroviruses & rhinoviruses.
 Other unusual bacteria
 Alloiococcus otitidis - Gram positive cocci
 Turicella otitidis – Gram positive bacilli

18. Mycobacterium OM
 Mycobacterium tuberculosis
 Incidence 0.04% - 0.9%
 Can get to ear by haematogenous route,
regurgitation through the eustachian tube,
through previously existing tympanic
membrane perforations, or direct extension
of a nasopharyngeal site of infection.

19. Evaluation of patient
 History of contact with TB.
 Culture and staining of ear fluid for AAFB.
 Chest X Ray, urinalysis and sputum
Microscopy & culture for AAFB.
 LP if CNS involvement suspected.
Treatment
6 – 9 month treatment with isoniazid,
rifampicin and pyrazinamide.

20. Parasites
 Ascaris worms have
been found in the
middle ear causing
chronic OM after
migrating from the
naso-pharynx via the
eustachian tube.

21. Treatment of OM
 Oral antibiotics.
 Surgical treatment by
Myringotomy. Allow
fluids to drain out can
be used with
Tympanostomy tubes.

22. Myringitis
 Inflammation of the tympanic
membrane
 Myringitis can be caused by bacteria
such as S.pneumoniae, M.
pneumoniae, H.influenzae or viruses
such as Herpes zoster and influenza.
 Bacterial infections are usually treated
with antibiotics.

23. Upper respiratory tract

24. Nose
 External region is composed of a framework
of bone & cartilage overlain with skin and
lined with mucous membrane. The external
nares lead to a vestibule lined with skin
bearing hairs for coarse filtering.
 Inner nasal cavity lies above the mouth and
communicates with the pharynx via 2
internal nares. 4 paranasal sinuses also open
into this cavity. The inner nose is also lined
by a mucous membrane which secretes
mucous. Its walls are thrown into a series of

25. Pharynx
 Muscular and lined with a mucous
membrane.
 Upper nasopharynx. Receives air from the
internal nares and also communicates, via 2
openings of the eustacian tubes, with the
ears. This is also the site of the adenoids.
 Oropharynx. Lies behind the mouth and is a
common passage way for the respiratory and
digestive tracts. The 2 pairs of tonsils are
found here.
 Lower laryngopharynx. The digestive and

26. Larynx
 This connects the pharynx and
trachea. The epiglottis, a cartilage
overlying the larynx, moves like a
trapdoor to close off the remainder
of the respiratory tract during
swallowing of food.

27. Respiratory immune defence mechanisms
Site Mechanism
Nose Hair
Mucous secretion
Nasopharynx Mucous secretion
Ciliated epithelium
Adenoids
Oropharynx Tonsils
Mucocilliary clearance
Saliva:
Secretary antibody
Lysozyme
Lactoperoxidase
Laryngopharynx Mucocilliary clearance
Mucosa Associated Lymphoid Tissue
(MALT)

28. Colonization resistance
Normal flora Respiratory pathogens that
can be carried
Transient colonisation
α haemolytic streptococci S. pyogenes Enterobacteriaceae
Neisseria species S. pneumoniae Pseudomonades
Diphtheroids H. influenzae Candida
Anaerobic cocci C. diphtheriae
Fusobacteria
Bacteroides
Micrococci

29. Nose swabs
Nasal carriage
 S.aureus including MRSA
 Lancefield group A streptococci
 C. diphtheriae
 Epistaxis – S.aureus carriage

30. Sinuses
 Frontal sinuses (in the forehead)
 Maxillary sinuses (behind the cheek
bones)
 Ethmoid sinuses (between the eyes)
 Sphenoid sinuses (behind the eyes)

33. Sinusitis
 Sinusitis, nasal discharge.
 Looking for: S.pneumoniae,
H.influenzae but may be caused by
‘S.milleri’ group and anaerobes
especially if the condition is chronic.
 Nose swabs are no good. Pus, antral
wash outs, nasopharyngeal swabs or
ethmoid biopsies needed.

34. Mucormycosis
 Caused by:
Rhizomucor,
Cunninghamella,
Apophysomyces,
Saksenaea,
Absidia, Mucor,
Syncephalastrum,
Cokeromyces,
and Mortierella.

35. Mucormycosis
 Most infections are life-threatening, and risk
factors, such as diabetic ketoacidosis and
neutropaenia, are present in most cases.
Severe infection of the facial sinuses, which
may extend into the brain, is the most
common presentation.
 Successful treatment requires correction of
the underlying risk factor or factors,
antifungal therapy with amphotericin B, and
aggressive surgery.
 Mucormycosis carries a very high mortality

36. Fungal balls
 Sphenoidal and maxillary fungal
balls
 Non-invasive
 Headaches
 Can lead to recurrent bacterial
infections and central nervous
system complications

37. Sphenoid fungal balls
Computed tomography scan of
the sinuses.
Axial view of sphenoid sinus
showing opacity, small
hyperdensities (white arrow) and
osteosclerosis (black arrow) of
the bone wall
Photography of the fungus ball, or truffle.

38. Maxillary fungal balls
Removal of fungal ball from maxillary sinus

39. Rarely seen nasal infections
Rhinoscleroma
 Caused by Klebsiella
rhinoscleromatis. Rare
form of chronic
granulomatous nasal
infection affecting nasal
passages and sinuses and
can include the larynx and
pharynx. Progressive –
tumour-like growths.
 Found in Eastern Europe,
Latin America, Central
Africa and South East
Asia.
Hebra nose

40. Rhinoscleroma
 Endemic to North and Central Africa, Central and
South America and Southeast Asia.
 Rhinoscleroma has been identified as an
opportunistic infection that can occur in patients
with HIV infections
 There are three histologic stages of development of
rhinoscleroma. In the catarrhal stage, the mucosa
contains non-specific inflammatory changes with
neutrophils, cellular debris and granulation tissue.
In the proliferative stage, there is an intense
infiltrate of plasma cells and large foamy
histiocytes termed "Mikulicz cells" which contain
numerous rod-shaped bacteria within their

41. Rhinoscleroma
 Diagnosis is usually made by the identification of
the Mikulicz cells in tissue biopsy. The bacteria
may be seen in H&E stained sections, but are
more easily identified with PAS, Geimsa or
Warthin-Starry stains.
 Therapy is with traditional antimicrobial therapy -
streptomycin, tetracycline and trimethoprim-
sulfamethoxazole which may successfully treat
early lesions. Prolonged high dose oral
ciprofloxacin has been successful in achieving
resolution in patients with extensive disease.
Surgical debridement may be necessary in cases of
airway obstruction.

42. Rarely seen nasal infections
Ozaenia
 Chronic atrophic rhinitis.
 Can destroy the mucosa –
characterized by purulent, chronic
foul smelling nasal discharge.
 Klebsiella ozaenae thought to be
the causative organism.

43. Rarely seen nasal infections
Rhinosporidiosis
 Originally thought to be
fungus
 It is a novel aquatic
protistan parasites
Mesomycetozoea
(DRIP clade)that infects
fish & amphibians as well
as man. Found in Eastern
Europe, South East Asia,
Central Africa & Latin
America.
Section of human nasal polyp stained
with periodic acid-Schiff (PAS) showing
Rhinosporidium seeberi cysts.

44. Rhinosporidiosis
 Slow growing tumour like masses –
usually leading to unilateral obstruction
and polyp formation.
 Diagnosis is by staining of tissue
biopsies.
 Treatment by surgical excision
although relapses are common (10%).
Antimicrobial therapy ineffective.

45. Tonsillitis/pharyngitis

46. Tonsillitis/pharyngitis
 Streptococcus pyogenes
Scarlet fever
Non-suppurative post streptococcal sequelae:- Rheumatic
Fever. Glomerulonephritis.
Occur 2 -3 weeks after infection
 Lancefield groups C & G
 Vincents organisms
 Viral – EBV, CMV, Enteroviruses, Adenovirus, Herpes
simplex, influenza viruses
 Non-toxigenic Corynebacterium diphtheriae
 Arcanobacterium haemolyticum
 Candida
 Neisseria gonorrhoeae
 H. parainfluenzae

47. S. Pyogenes
Determinants of pathogenicity
Lipoteichoic acid Mediates adherence to bucchal mucosa,
complexes with M protein and binds to
fibronectin
M Protein Anti-phagocytic
Pyrogenic exotoxin (erythrogenic toxin)
A, B and C
All phage mediated.Dermal reactivity thought
to be a hypersensitivity reaction
Streptolysin O Extracellular
Oxygen labile
Antigenic
Membrane injury to cells
Streptolysin S Cell bound
Oxygen stable
Leucotoxic (after ingestion) to cell
NADase Especially produced by nephritogenic
strains (eg M12)
DNAase
A, B, C and D
Antigenic

48. Association of M types with disease
M type Pharyngitis Pyoderma
1 +++ ?
2 0 +++
3 ++ +/-
4 +++ +/-
12 ++++ +/-
25 ++ +/-
49 ++ ++++
55 0 +++
57 0 ++

49. Scarlet fever
 Sore throat, fever, bright red tongue and fine
pinkish-red rash on the body that feels like
sandpaper to touch. It may start in one
place, but soon spreads to many parts of the
body, commonly the ears, neck, chest,
elbows, inner thighs and groin.
 The rash does not normally spread to the
face, but the cheeks become flushed and the
area just around the mouth stays quite pale.
 Streptococcal pyrogenic exotoxin A (SPE A)
(scarlet fever toxin)
 Associated with M types:1, 3, 4, 6, 18, and 22

50. S. Pyogenes
Non-suppurative sequelae
 Rheumatic fever
 Causes arthritis, carditis, Sydenham chorea,
erythema marginatum and sub-cutaneous
nodules
 Associated with phayngitis attack 3-4 weeks
previously
 Common in children 6 -15 years old
 Thought to be caused by antibody cross
reactivity. Characteristic rheumatic
granulomata develop in the connective
tissues and heart – Aschoff’s nodules.
 Repeated attacks lead to valvular disease

51. S. Pyogenes
Non-suppurative sequelae
 Acute glomerulonephritis
 7-14 days post pharyngitis (or 14 -21
days post pyoderma)
 Immune complexes in renal tubules
 Associated with M types: 12 from
pharyngeal strains but 49 from
pyoderma
 Clinical symptoms – Oedema, oliguria,

52. Complications of throat infections
 Quinsy
 Lemierre’s disease – infection of
the jugular vein which can lead to
septicaemia. Caused by
Fusobacterium necrophorum.
 Epiglottitis – Haemophilus
influenzae

53. Fusobacterium necrophorum
 Recurrent or persistent sore throat
 3 -5 days anaerobic incubation on
supplemented blood plates such as
Fastidious Anaerobic Agar.
 MAST-ID ring resistant to
vancomycin & sensitive to
kanamycin & colistin.
 Colonies fluoresce green under UV
(300-412 nm)

54. Diphtheria
 Diphtheria is an upper
respiratory tract illness
characterized by sore throat,
low fever, and an adherent
membrane (called a
pseudomembrane on the
tonsils, pharynx, and/or nasal
cavity.
 Diphtheria toxin produced by
C. diphtheriae, can cause
myocarditis, polyneuritis, and
other systemic toxic effects. A
milder form of diphtheria can
be restricted to the skin.

56. Metachromatic granules

57.  Corynebacterium
diphtheriae
4 biotypes –
Gravis, mitis,
intermedius & belfanti

58. Diphtheria
Gel diffusion test (ELEK plate) for C.diphtheria
toxin.
Outer strains are non-toxigenic, those in the
centre show toxin production. The anti-toxin
had been absorbed with non-toxic proteins
obtained from a non-toxigenic culture and thus
behaved as a monospecific antiserum. The
intersection of the bands with the bacterial
growth is removed some distance from the
piece of filter paper impregnated with
antiserum because horse anti-toxin has been
employed, which inhibits the precipitin
reaction in the region of antibody excess. Note
that the lines of precipitate generated by the 2
toxigenic strains merge to form arcs, indicating
that the toxins elaborated are immunolog
ically identical. (King et al, Am. J. Pub. Health,
1949, 39, 1314).

59.  The Diphtheria Toxin
(DTx) Monomer. A (red)
is the catalytic domain; B
(yellow) is the binding
domain which displays the
receptor for cell
attachment; T (blue) is the
hydrophobic domain
responsible for insertion
into the endosome
membrane to secure the
release of A. The protein is
illustrated in its "closed"
configuration.

60. Oral thrush
 Overgrowth of
Candida albicans due
to:
 Broad spectrum
antibiotic therapy
 Impaired immunity –
eg leukaemia,
lymphoma, AIDS
 Diabetes

61. Whooping cough
 The first recorded
outbreaks were in the 16th
century
 B. pertussis was isolated
in pure culture in 1906 by
Jules Bordet and Octave
Gengou
 The term whoop
originates from the
inflammation and
swelling of the laryngeal
structures that vibrate
when there is a rapid
inflow of air during
inspiration. Jules Bordet

62. Vaccines
 Historically, the whooping cough vaccine has been
administered as a merthiolate-killed bacterial cell
suspension which is part of the DTP vaccine
 Children are vaccinated at two, three and four months and
again before they start school
 Immunity is not lifelong and older teenagers and adults are
still susceptible to whooping cough
 Unfortunately, about 20% of the children that receive the
whole cell vaccine experience mild side effects. About 0.1%
of infants experience convulsions soon after receiving the
vaccine and in a very small number of cases (1 in 150,000?)
severe or irreversible brain damage may occur.
 Acellular pertussis has fewer side effects than the whole cell
vaccine

63. Methods for detection
 Culture
 Direct immunofluorescence
 PCR
 Serology
 B. pertussis can only be recovered for
the first 3 weeks of infection
 PCR can be of use for a further 3 weeks
 Serology

64. Pernasal swab
 With the patient's head
immobilized, a swab
should be gently
inserted into the nostril
until it reaches the
posterior nares and is
then left in place for a
few seconds. The
tickling sensation of
the swab usually
induces a cough.

65. Bordetella pertussis

66. Whooping cough
 Bordetella pertussis
3 stages:
 Colonisation
 Toxaemic
 Recovery

67. 1-Colonisation stage
 Catarrhal stage. Fever & cough, worse at
night. ‘Runny nose’ and sneezing.
 Organism readily isolated from pharyngeal
cultures.
 Severity and duration of illness can be
reduced by antibiotic treatment
(erythromycin).
 Adherence mechanisms - Filamentous
Haemagglutinin (FHA), a fimbrial like
structure and cell bound Pertussis Toxin

68. 2-Toxaemic stage
 Spasmodic (Paroxysmal) stage.
Paroxysms of coughing followed by
inspiratory whoop.
 Apnoic attacks & cyanosis.
 B.pertussis rarely recovered.
 Antimicrobial agents no effect on
progress of disease.

69. 3-Recovery stage
Gradual abatement of disease
The cough is very persistent, long after
infection is past and may last for 2 or 3
months. It was called 'the 100 days' cough'.
Complications:
 Bronchopneumonia (commonly with H.
influenzae or S. pneumoniae.
 Atelectasis leading to bronchiectasis.
 Convulsions leading to brain damage.