Infections of the Ears

GROUP 9 3MB
Kathleen Cedillo
Richelle Grace S.
Pazzibugan
Alane Biffany Tan
 Anatomy

• Outer Ear

• Middle
Ear
• Inner Ear
 EXTERNAL EAR
External Acoustic Meatus
 Extends from the concha to the
tympanic membrane.
 Lateral part is cartilaginous and
continuous with the auricle; the longer
medial part is bony.
 Cartilaginous part of the meatus is
slightly concave anteriorly, and a
speculum may be inserted more readily
when the auricle is pulled backward
and upward.
 Lined by the skin of the auricle, which
presents hairs, and sebaceous and
ceruminous glands.

Sensory Innervation and Blood

Supply.
 Supplied by the auriculotemporal
nerve and the auricular nerve.
 Posterior auricular and superficial
temporal arteries of the external
carotid artery provide the blood supply.
 EXTERNAL EAR
Tympanic Membrane.
 The ear drum separates the
external meatus from the
tympanic cavity.
 The larger portion of the
membrane is its tense part;
the anterosuperior comer, or
flaccid part, is bounded by
anterior and posterior mallear
folds. The tympanic membrane
is set very obliquely.
 Lateral surface is concave,
and its deepest point is the
umbo.
 The membrane can be
examined in vivo by a
speculum.
 The tympanic membrane is
highly sensitive
 MIDDLE EAR
 Consists largely of an air space in the temporal bone
 The tympanic cavity and auditory tube develop as a recess of
the embryonic pharynx. Mucous membrane covers the structures
in the tympanic
Auditory cavity.
Ossicles, Joints, and Muscles.
 The ossicles are the malleus (hammer), incus (anvil), and stapes
(stirrup). The malleus presents a head and neck; a handle
(manubrium) and lateral process, embedded in the tympanic
membrane; and an anterior process, attached to the petrotympanic
fissure. The incus presents a body, short crus, and long crus. The
stapes presents a head, anterior and posterior crura, and a base or
footplate, which is attached by an annular ligament to the margin of
the oval window.
 The joints are saddle and ball-and-socket synovial joints,
respectively.
 Tensor tympani arises from the cartilaginous part of the auditory
tube, enters a semicanal, turns laterally around the cochleariform
process, and is inserted on the handle of the malleus.
 Supplied by the facial nerve, the stapedius draws the stapes
laterally.
 INTERNAL EAR
 Situated within the petrous part of the temporal bone, consists of a complex
series of fluid-filled spaces, the membranous labyrinth, lodged within a similarly
complex cavity, the bony (osseous) labyrinth.
 Cochlea is the essential organ of hearing. Other portions (the utricle and
semicircular ducts) of the internal ear constitute the vestibular apparatus,
although equilibrium is also maintained by vision and proprioceptive impulses.
Osseous Labyrinth
 Comprises a layer of dense bone (otic capsule) in the petrous part of the
temporal bone and the enclosed perilymphatic space, which contains a fluid
very similar to extracellular fluid, the perilymph. The perilymphatic space
consists of a series of continuous cavities: semicircular canals, vestibule, and
cochlea

Semicircular canals
 The anterior, posterior, and lateral semicircular canals are at right angles one
to another.

Vestibule
 Restricted to the middle part of the bony labyrinth, immediately medial to the
tympanic cavity.
 Contains the utricle and saccule of the membranous labyrinth.
Cochlea
 Its base lies against the lateral end of the internal acoustic
meatus, its basal coil forms the promontory of the middle ear, and
its apex is directed anterolaterally.

Perilymphatic duct
 The perilymphatic duct, or aqueduct of the cochlea, is situated
in a bony channel, the cochlear canaliculus, and is frequently said
to connect the scala tympani with the subarachnoid space.

Membranous Labyrinth
 Lies within the bony labyrinth and contains a different fluid,
endolymph.
 Consists of a series of continuous cavities: semicircular ducts,
utricle and saccule, and cochlear duct.
Semicircular ducts
Anterior, posterior, and lateral semicircular ducts are situated
eccentrically in the corresponding canals.

Utricle and saccule

Lie in the vestibule and communicate with each other by
utricular and saccular ducts. The utricle has five openings for the
semicircular ducts. The saccule is joined to the cochlear duct by
the ductus reuniens.

Cochlear duct
Winds from the saccule to the apex of the cochlea, where it ends
blindly and extends from the osseous spiral lamina to the wall of
the cochlea. Its anterior and posterior walls are the vestibular
and basilar membranes, respectively.
1. External ear
infections:
 Otitis Externa

- Acute Otitis
Externa
- Chronic Otitis
Externa

2. Middle ear infections

 Otitis Media
 OTITIS EXTERNA
 Acute Otitis Externa
Epidemiology & Pathogenesis
 Higher frequency in warm, humid climates ; more
common in swimmers due to local maceration of the canal
skin

 Alkaline pH of swimming pools affects the susceptibility

of the external auditory canal to bacterial overgrowth and
subsequent infection.

 Trauma- removal of cerumen by cotton-tipped applicators

or other instrumentation predisposes the canal skin to
maceration.

 Other causative factors: hearing aids, absence of

cerumen, a narrow and external canal with poor self-
cleaning ability, foreign bodies and allergy to
mnedications
Acute Otitis Externa
 Signs and Causative Agents
Symptoms
 straightforward in  Pseudomonas
adult; confusing in aeruginosa
child  Streptococcus
 Otalgia (Earache) and
fever pneumoniae
 Pruritus(Itching)  Haemophilus
 Erythema(Redness of influenzae
the skin)  Beta-hemolytic
 Edema (external Streptococci
auditory canal) ==
Hearing loss  Staphylococcus spp.
 Dilemma in child is  Proteus
evident in younger
 Escherichia coli
 Other gram negative
rods and anaerobes
Diagnostic Workup
 Gram staining - shows more than one kind of gram-
negative rod
 If only one grows out in culture, the other may be
anaerobes
 External ear drainage no cultures performed
 24-48 hr culture
Treatment Options

 Risk-factor modification- reducing trauma to the

external auditory canal by refraining from the use of
cotton-tipped swabs and eliminating exposure to
water by using earplugs or cotton balls.
 Meticulous cleaning under the microscope- use of a
suction aspirator for symptomatic relief and for topical
medicine to reach the skin.
 Topical antibiotics that contain boric or acetic acid to
decrease the pH of the canal

● Neomycin- active against S. aureus, Proteus, Klebsiella,

E.coli
but not against Pseudomonas

● Polymyxin B or E- active against Pseudomonas, E.coli,

Klebsiella, but not against Proteus or many gram
positives.

● Gentamicin- active against Pseudomonas.

● Cortisporin suspension (polymixin B-bacitracin-neomycin-

hydrocortisone)

 Antibacterial eardrops

● Dilute 0.25% acetic acid

 OTITIS EXTERNA
 Chronic Otitis Externa
Epidemiology & Pathogenesis

 Skin changes of acanthosis, increased size of rete

pegs, inflammation around apocrine glands, and
absence of sebaceous glands are seen

 Evolve from underlying skin disorders such as

seborrheic and atopic dermatitis

 Prolonged treatment with antimicrobial drops and

steroid creams and topical allergies (neomycin).
 Signs and Symptoms

 Skin is thickened and canal may be stenosed.

 Lichenification, excoriations, and dry adherent debris
(keratosis)
 Conductive hearing loss  progression to
postinflammatory mediaal canal fibrosis.
 History of underlying skin disorder or diabetes

Causative Agents

 Gram-negative bacilli  Proteus.

Chronic Otitis Externa
Diagnostic Workup

 Gram staining
 Culture. Biopsy if there is persistent granulation, ulcer,
and lack of response to therapy.

Treatment Options

 Risk-factor modification
 Meticulous cleaning under the microscope- use of a
suction aspirator for symptomatic relief and for topical
medicine to reach the skin.
 Topical antibiotics that contain boric or acetic acid to
decrease the pH of the canal should be delivered in high
nontoxic concentrations

● Neomycin- active against S. aureus, Proteus,

Klebsiella, E.coli but not against Pseudomonas

● Polymyxin B or E- active against Pseudomonas, E.coli,

Klebsiella, but not against Proteus or many gram
positives.

● Gentamicin- active against Pseudomonas.

● Cortisporin suspension (polymixin B-bacitracin-

neomycin-
hydrocortisone)

 Direct injection of corticosteroids for persistent edema of

the canal skin
 ACUTE OTITIS MEDIA
Epidemiology & Pathogenesis

 Inflamation of the middle ear

 Most common diseases of childhood

 Include age < 6 years, male gender, group day care,

lack of breast feeding, secondhand smoke exposure,
craniofacial growth abnormalities

 Presence of frequent upper respiratory tract viral

infections

 Factors: Bacterial infection of the middle ear space and

eustachian tube dysfunction
ACUTE OTITIS MEDIA
 Signs and Symptoms
 Otalgia
 Earache with high pressure  Rupture of eardrum
 Edema
 Fever, Dizziness, Nausea and Vomitting
 Hearing loss
 Bulging, opaque tympanic membrane with some
degree of erythema that later becomes thick
Causative Agents
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
 Streptococcus pyogenes
 Staphylococcus aureus
 Gram-negative pathogens
 Group B streptococci and gram-negative bacilli
Diagnostic Workup

 Audiogram and CT scan

 Culture from otorrhea
 Typanocentesis, removal of fluid behind the eardrum

Treatment Options

 Myringotomy if middle ear is not draining

 Addition of steroid therapy to prevent hearing loss and
labyrinthitis ossificans.
Normal right tympanic Bulging right tympanic
membrane and middle membrane in acute otitis
ear media
 OTITIS INTERNA
Epidemiology & Pathogenesis

 Other known as Labyrinthitis

 Occurs when toxic mediators reach the membranous

labyrinth

 Incidence is unknown but is uncommon.

OTITIS INTERNA
 Signs and Symptoms
 Sudden onset of mild to moderate hearing loss
 Occasionally vertigo
 Otalgi
 Fever, Dizziness, Nausea and Vomitting

Causative Agents
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
Diagnostic Workup
 Audiogram and CT scan
 Culture from otorrhea
 Typanocentesis, removal of fluid behind the eardrum

Treatment Options

 Myringotomy if middle ear is not draining

 Addition of steroid therapy to prevent hearing loss and
labyrinthitis ossificans.
Infections of the
mouth
GROUP 9 3MB
Kathleen Cedillo
Richelle Grace S.
Pazzibugan
Alane Biffany Tan
-The mouth is composed of
the upper and lower lip,
teeth, gums, cheeks, tongue,
palate, tonsil, uvula and
incisors.

-Has a wet, warm and dark

environment.
 Normal Flora
 Epidemiology
-Common and fatal during the 19th century

 Signs and symptoms

-sore throat
-fever
-rash on face
-circumolar palor
-blanching erythema
-punctuate elavations around the hair follicles
 Signs and symptoms
-Dequamation
-strawberry tongue
-raspberry tongue

 Etiologic agent
-S.pyogenes
-or group A β-hemolytic streptococci
 Pathogenesis

- Excrete hemolyzing enzymes and

toxins
- Production of erythrogenic toxin
- Accompanies streptoccocal
pharyngitis
 Laboratory Diagnosis
-throat swab
- Blood agar Media

- Trypticase-soy broth

- Brain broth

 Treatment
-Oral penicillin V
-Parenteral benzylpenicillin
 Epidemiology
-Very common infectious disease in US

 Signs and symptoms

-Burning in the throat
-vulvitis
-Swollen glands in throat
-sore throat
 Etiologic agents
-Neisseria gonorrhea

 Pathogenesis
- Resists phagocytosis
- Attacks the mucous membrane
- Produce acute suppuration
- Invades tissues
 Laboratory Diagnosis
- Throat Swab
- Gram stain
- Methylene blue stain
- Immunoflourescent staning
- Thayer-Martin Medium
- Incubated in candle jar
- Fermentation test
 Treatment

 -Cipro® XR 500 mg a single dose, or

 Levaquin® 500 mg a single dose, or

 Tequin® 400 mg a single dose

 Epidemiology

- Often affects children Under Age 5

- Occurs 19 out of every 10,000 kids in
the US.
- Common on Koreans and Japanese
 Signs and Symptoms
- Fever (39 C)
- Redness of the eye
- a rash on the stomach, chest, and genitals
- red, dry, cracked lips
- swollen tongue with a white coating and
big red bumps
- sore, irritated throat
 Signs and Symptoms
- swollen palms of the hands and soles
of the feet with a purple-red color
- swollen lymph nodes
- Crack lips
- Fever
- Reddening of eyes
 Etiologic Agent/s
- S. Aureus and / s. pyogenes

 Pathogenesis
-cause severe aneurysmal dilations
- Damages the coronary arteries

- changes in the mucous membranes that

line the lips and mouth and by the

enlarged and tender lymph nodes.
 Laboratory Diagnosis
- Gram stain
- Blood agar Plate
- Coagulase test
- Tellurite Medium
- Serologic test
- Echocardiogram
 Treatment

- intravenous doses of gamma

globulin
- Salicylate therapy
- high dose of aspirin
- Corticosteroids
 Epidemiology

- Known as silk road disease

- rare in the United States
- the disease affects more men than
women
- Common on people of age 20-30 yrs
 Signs and Symptoms
- Mouth sores
- Heat
- Pain
- swelling
 Etiologic agent
- Streptococcus sanguinis

 Pathogenicity

- Damages the veins

- Attacks the tissues
 Laboratory Diagnosis
- Blood samples
- Throat swab
- Blood agar plate
 Treatment
- 1 mg/kg/d oral prednizone
- Infliximab
- Interferon alfa-2a
- Thalidomide
- Corticosteroids
- Azathioprine
- Cyclosporine
- Colchicine
 Epidemiology

- most commonly seen in children

- Most common reason of children’s
medical visit
- About 25 percent of sore throat is
caused by strep bacteria
- Usually winter or spring
 Signs and symptoms
- difficulty in swallowing
- Pain may spread to the ears.
- Redness of throat
- Swollen tonsils
- High temperature may occur
- Lymph nodes may occur
 Signs and syndromes
- Foul breath
- Tonsils are coated
- May feel ill

 Etiologic Agent
- Group A streptococcus
 Pathogenesis

- Abscess develops
 Laboratory Diagnosis
- SBAP, Chocolate Agar Medium
- Throat culture
- Rapid strep test
- Anti-streptolysin O or ASO titer
- Complete Blood count
- Monospot test
 Treatment

- Drink warm liquids

- Gargle water with salt
- Sucking on hard candies or throat
lozenges
- Cool mint vaporizer
- Acetaminophen
 Physiology of mouth
 1500 ml saliva is secreted daily from
glands in the mouth
 IgA molecules protect against
invasion
 Leukocytes are present
 Normal flora
Environment Numbers

Saliva 40 billion/ mL
110 billion/mL

Inner cheek epithilium 5- 25 bacteria/ cell

Tongue surface 100 bacteria/ cell

Gingival crevice 16 billion/g

40 billion/g

plaque 25 billion/g
46 billion/g
 Bacterial diseases in teeth
 Dental carries

 Periodontal disease

 Trench mouth
Dental carries
 cariosus means “rotten”

 Common name: tooth decay

 Most common infectious disease

 80% of tooth extractions are of tooth loss due to carries

 Results from microbial acid and plaque formation

 Incubation: 1 to 24 months before cavity is detectable

 Symptoms: toothache, discoloration, roughness, breaking of

tooth during chewing.

 Agents: Streptococcus mutans, Lactobacillus acidophilus,

and Lactobacillus casei
 Pathogenesis
 Formation of cariogenic plaque (plaque that causes tooth decay) is
the adherence of oral streptococci to specific on the tooth pellicle.

 If dietary sucrose is present, S.mutans attaches to the bacterial mass

and produces glucans from sucrose through the action of
extracellular enzymes

 Sucrose is split by the enzymes to the monosaccharide glucose and

fructose. The glucose is polymerized, yielding glucan, and the
fructose is metabolized, producing lactic acid.

 Glucans bind the organisms together and to the tooth, and make the
plaque impenetrable to saliva

 pH of cariogenic plaques drops to below 5 within minutes

 Calcium phosphate of teeth dissolves because the acidity of plaque is

more than a 100-fold increase

 After food leaves the mouth, the pH slowly returns to its neutrality; if
the pH is delayed in return of neutrality, it is due to the ability of
S.mutans to store a portion of its food as an intracellular, starchlike
polysaccharide that is later metabolized with the production of acid.
 Epidemiology
 It varies markedly depending mainly on
dietary sucrose and access to
preventive dental care
 Hereditary also plays an important role
because some individuals inherits
resistance to this disease
 Young people are generally much more
susceptible than older people because
the pits and fissures that are sites for
dental caries wear down in time
Treatment and Prevention
 Using of sealant in pits and fissures
 Reduce intake of sucrose and other
refined dietary carbohydrates
 Careful flossing and tooth brushing
 Supplemental fluoride
 Mechanical removal of plaque
Periodontal disease
 Meaning around the tooth
 Chronic inflammatory process involving
the gums and tissues around the roots of
the teeth
 Develops slowly over many years
 Important cause of tooth loss from middle
age onward
 Incubation: months or years
 Agents: plaque and tartar
 Symptoms: asymptomatic until advance
cases, bleeding gums, loosening of the
teeth, discoloration from yellowish to black
that occurs at the base of the teeth
 Pathogenesis
 plaque forms on teeth at the gum margin, especially in hard to
clean areas between the teeth

 Plaque gradually extends into gingival crevice

 Bacterial products incite an inflammatory and immune

response manifested by swelling and redness of the gingiva

 If it is in small population, it can be stopped by the immune

system of the body

 In large population, it releases the enzymes collagenase and

hyaluronidase, which weaken the gingival tissue and cause the
gingival crevice to widen and deepen

 As the plaque enlarges, Porphyromonas gingivalis increases

 The membrane that attaches to the root of the tooth to the

bone weakens, and the bone surrounding the tooth gradually
softens
Epidemiology
 Mainly a disease of those over 35
years old
 After 65 years old, 90% of individuals
have some degree of periodontal
disease
 Immunodeficient individuals are at
higher risk of severe diseases
Treatment and prevention
 Careful flossing and toothbrushing
 Yearly polishing and removal of
calculus
 Cleaning of inflamed gingival crevice
 In advance cases, surgery is required
to expose and clean the roots of the
teeth
 Avoid buildup of plaque
Trench mouth
 Also known as Vincent’s disease or acute necrotizing
ulcerative gingivitis (ANUG)
 Sever, acute condition distinct from other forms of
periodontitis
 Rampant among soldiers
 Not contagious
 Polymicrobial infection
 Far more common among smokers than among
nonsmokers
 Agents: Borrelia vincentii (a spirochete), Bacillus
vincentii (a fusiform), and other anaerobes
 Symptoms: abrupt onset of fever, painful bleeding
gums, and foul mouth odor
Pathogenesis
 Spirochetes and fusiform are presumed to
act together to destroy tissue, but the
precise mechanisms are unknown

 Plaque is always present, but its bacterial

composition shows much large number of
spirochetes and other anaerobes than in
chronic periodontal disease

 The spirochetes invade the tissue causing

necrosis and ulceration, mainly of the
gums between the teeth
Epidemiology
 All ages are susceptible in
association with poor mouth care,
malnutrition, or immunodeficiency
Prevention and treatment
 Daily brushing and flossing
 Twice a year of professional cleaning
 Rinsing several times a day with a
hydrogen peroxide solution