Ear, Nose and Throat

infections
Ear canal
 Ear canal 2.5 cm cul de
sac.
 Cartilaginous covered
by layers of sebaceous
and apocrine glands and
hair.
 The glands produce a
thin layer of ceruman.
 Defence mechanisms of ear
 Outer ear
 Hair
 Ceruman

 Internal ear
 External bony part of the labyrinth has
perilymph
 Internal membrane part contains endolymph
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.
 Perforation of tympanic
membrane due to
insertion of a 'q' tip.
This is likely to result in
both an otitis media and
otitis externa
 Otitis externa
 Acute localised otitis externa
 Acute diffuse otitis externa
 Chronic otitis externa
 Malignant otitis externa
 Ear swabs
 Culture of ear swabs

 Used for OE not very useful for OM unless

fluid from the middle ear is swabbed
 Neonatal screening
 Acute OE
 Majority of infections are due to bacteria –
Staphylococcus aureus, Pseudomonas
aeruginosa, anaerobes
 Fungal infections account for only 10%
 Acute OE
 Acute localised OE usually caused by S.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
S.aureus, pseudomonas and anaerobes.
 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
gentamicin used or fluoroquinolones.
 Chronic otitis externa
External auditory canal with

Aspergillus overgrowth manifesting
 Chronic OE is usually
as a cottony matrix topped by small caused by colonisation
black balls.
by coliforms or fungi
and is best treated by
topical cleansing rather
than antibiotic
treatment.
 Rarely caused by
syphilis or leprosy
 Malignant otitis externa
 Malignant external otitis with pus
draining from the necrotic ear canal
 Life threatening condition
and underlying osteomyelitic bone. affecting diabetics, the
immunocompromised
and elderly.
 Severe necrotising
infection of soft tissues,
bones, blood vessels and
cartilage with risk of
neurological involvement
and facial paralysis.
 Malignant otitis externa
 The patient requires hospital admission and
treatment with high dose antibiotics, surgery to
debride dead tissue and occasionally
hyperbaric treatment.
 Non-bacterial cause of OE
 Ramsey Hunt Syndrome – Herpes Zoster
Oticus. Severe otalgia, facial paralysis and
varicelliform rash over the pinna. Treated with
antivirals.
Aspergillus niveus
 Otitis media
 Occurs between the ear drum and the inner ear
and includes the eustacian 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.
 Acute Otitis media
 Usually caused by migration of bacteria from the
naso-pharynx up the eustacian 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
eustacian 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.
 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,
enterobactericae and anaerobic Gram negative
non-sporing rods such as prevotella,
fusobacteria, porphyromonas and bacteroides .
 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 pseudomonads 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.
 Mycobacterium OM
 Mycobacterium tuberculosis
 Incidence 0.04% - 0.9%
 Can get to ear by haematogenous route,
regurgitation through the eustacian tube,
through previously existing tympanic
membrane perforations, or direct extension of
a nasopharyngeal site of infection.
 Clinical presentation
 Insidious onset with painless otorrhoea.
 Multiple tympanic membrane perforations.
 Abundant pale granulation tissue in ear.
 Early severe hearing loss.
 Bone necrosis.
 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.
 Other unusual bacteria
 Alloiococcus otitidis - Gram positive cocci
 Turicella otitidis – Gram positive bacilli
Parasites
 Ascaris worms have
been found in the
middle ear causing
chronic OM after
migrating from the
naso-pharynx via the
eustachian tube.
 Treatment of OM
 Oral antibiotics.
 Surgical treatment by
Myringotomy. Allow
fluids to drain out can
be used with
Tympanostomy tubes.
 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.
Upper respiratory tract
 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
folds causing air to around and facilitate the trapping
of particles in mucous.
 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 respiratory
tracts diverge here.
 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.
 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)
 Colonisation resistance
Normal flora Respiratory pathogens that Transient colonisation
can be carried

α haemolytic streptococci S. pyogenes Enterobactericiae

Neisseria species S. pneumoniae Pseudomonads
Diphtheroids H. influenzae Candida
Anaerobic cocci C. diphtheriae

Fusobacteria

Bacteroides

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

 Epistaxis – S.aureus carriage

 Sinuses
 Frontal sinuses (in the forehead)

 Maxillary sinuses (behind the cheek bones)

 Ethmoid sinuses (between the eyes)

 Sphenoid sinuses (behind the eyes)

 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.
 Mucormycosis
 Caused by:
Rhizomucor,
Cunninghamella,
Apophysomyces,
Saksenaea, Absidia,
Mucor,
Syncephalastrum,
Cokeromyces, and
Mortierella.
 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 rate (50-
85%).
 Fungal balls
 Sphenoidal and maxillary fungal balls

 Non-invasive
 Headaches
 Can lead to recurrent bacterial infections and
central nervous system complications
 Surgery
 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 Photography of the fungus ball, or truffle.
bone wall
Maxillary fungal balls

Removal of fungal ball from maxillary sinus

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
 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 cytoplasm. In the last stage,
there are variable degrees of fibrosis. Mikulicz cells are
characteristically absent.
 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.
 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.
 Rarely seen nasal infections
Rhinosporidiosis
 Originally thought to be
fungus
 It is a novel aquatic
protistan parasites
Mesomycetozoea (DRIP
clade)that infects fish &
Section of human nasal polyp stained amphibians as well as man.
with periodic acid-Schiff (PAS) showing Found in Eastern Europe,
Rhinosporidium seeberi cysts. South East Asia, Central
Africa & Latin America.
 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.
Tonsillitis/pharyngitis
 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
 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) All phage mediated.Dermal reactivity thought
A, B and C 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 Antigenic
A, B, C and D
 Association of M types with disease
M type Pharyngitis Pyoderma
1 +++ ?
2 0 +++
3 ++ +/-
4 +++ +/-
12 ++++ +/-
25 ++ +/-
49 ++ ++++
55 0 +++
57 0 ++
 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
 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
 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,
hypertension
 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
 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)
 API ID32
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.
Metachromatic granules
 Corynebacterium
diphtheriae
4 biotypes –
Gravis, mitis,
intermedius & belfanti
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).
 Requires lysogeny by
beta phage to produce
toxin.

 Toxin can also be

produced by C.ulcerans
& C.pseudotuberculosis
 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.
Oral thrush
 Overgrowth of Candida
albicans due to:
 Broad spectrum
antibiotic therapy
 Impaired immunity – eg
leukaemia, lymphoma,
AIDS
 Diabetes
 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
 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
 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
 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.
Bordetella pertussis
 Whooping cough
 Bordetella pertussis
3 stages:
 Colonisation

 Toxaemic

 Recovery
 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 (PTx).
 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.
 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.