Infections of the Ears

GROUP 9 3MBKathleen Cedillo

Richelle Grace S. PazzibuganAlane Biffany Tan

Anatomy

• The external ear (pinna) serves to protect the tympanic membrane (eardrum), as well to collect and direct sound waves through the ear canal to the eardrum.

• The canal contains modified sweat glands that secrete cerumen, or earwax.

• Too much cerumen can block sound transmission. 

OUTER EAR

Anatomy

• Eardrum is an air-filled cavity (tympanic cavity) carved out of the temporal bone. • It connects to the throat/nasopharynx via the Eustachian tube. • This ear-throat connection makes the ear susceptible to infection (otitis media). • Adjoining the eardrum are three linked, movable bones called "ossicles," which convert the sound waves striking the eardrum into mechanical vibrations.

MIDDLE EAR

Anatomy

• The front portion is the snail-shaped cochlea, which functions in hearing. 

• The rear part, the semicircular canals, helps maintain balance. 

• Interconnecting the cochlea and the semicircular canals is the vestibule.

INNER EAR

1. External ear infections:Otitis Externa

- Acute Otitis Externa- Chronic Otitis Externa

2. Middle ear infectionsOtitis Media

3. Internal ear infectionsOtitis Interna

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 medications

• Straightforward in adult; confusing in child

• Otalgia (Earache) and fever • Pruritus(Itching)• Erythema(Redness of the

skin)• Edema (external auditory

canal) == Hearing loss• Dilemma in child is evident

in younger• Narrowing of the canal &

swelling of soft tissues

Signs and Symptoms Causative Agents

Pseudomonas aeruginosaPseudomonas aeruginosa Staphylococcus aureusStaphylococcus aureus Streptococcus pneumoniaeStreptococcus pneumoniae Haemophilus influenzaeHaemophilus influenzae Beta-hemolyticBeta-hemolytic Streptococci Streptococci ProteusProteus Escherichia coliEscherichia coli Other gram negative rods Other gram negative rods

and anaerobesand anaerobes

Acute Otitis Externa

Redness of the pinna

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 OptionsTreatment Options

Risk-factor modification- reducing trauma to the external auditory Risk-factor modification- reducing trauma to the external auditory canal by refraining from the use of cotton-tipped swabs and canal by refraining from the use of cotton-tipped swabs and eliminating exposure to water by using earplugs or cotton balls.eliminating exposure to water by using earplugs or cotton balls.

Meticulous cleaning under the microscope- use of a suction Meticulous cleaning under the microscope- use of a suction aspirator for symptomatic relief and for topical medicine to reach aspirator for symptomatic relief and for topical medicine to reach the skin.the skin.

• Topical antibiotics that contain boric or acetic acid to decrease the pH of the canal

● Neomycin- active against S. aureus, Proteus, K. pneumoniae, E.coli but not against P.aeruginosa

● Polymyxin B or E- active against P.aeruginosa, E.coli, K. pneumoniae, but not against Proteus or many gram positives.

● Gentamicin- active against P.aeruginosa.

● Cortisporin suspension (polymixin B-bacitracin-neomycin- hydrocortisone)

• Antibacterial eardrops

● Dilute 0.25% acetic acid

● household vinegar and rubbing alcohol

OTITISOTITIS EXTERNA EXTERNA Chronic Otitis ExternaChronic Otitis Externa

Epidemiology & Pathogenesis

Changes of skin, 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).

• Skin is thickened and canal may be stenosed.• Lichenification, excoriations, and dry adherent debris (keratosis) • Conductive hearing loss progression to postinflammatory medial

canal fibrosis.• Obstruction of the ear canal & invasion of soft tissues.

Signs and Symptoms

Causative Agents

Gram-negative bacilli Gram-negative bacilli Proteus.Proteus.

Chronic Otitis Externa

Lichenification of the auditory canal

Diagnostic WorkupDiagnostic Workup

Gram staining Gram staining Culture. Biopsy if there is persistent granulation, ulcer, and lack of Culture. Biopsy if there is persistent granulation, ulcer, and lack of

response to therapy.response to therapy.

Treatment OptionsTreatment Options

Risk-factor modificationRisk-factor modification Meticulous cleaning under the microscope- use of a suction Meticulous cleaning under the microscope- use of a suction

aspirator for symptomatic relief and for topical medicine to reach aspirator for symptomatic relief and for topical medicine to reach the skin.the skin.

• Topical antibiotics that contain boric or acetic acid to decrease the pH of the canal

● Neomycin- active against S. aureus, Proteus, K. pneumoniae, E.coli but not against P.aeruginosa

● Polymyxin B or E- active against P.aeruginosa, E.coli, K. pneumoniae, but not against Proteus or many gram positives.

● Gentamicin- active against P.aeruginosa.

● Cortisporin suspension (polymixin B-bacitracin-neomycin- hydrocortisone)

• Direct injection of corticosteroids for persistent edema of the canal skin

ACUTE OTITIS MEDIAEpidemiology & 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

• 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

Signs and Symptoms

Causative Agents

Streptococcus pneumoniaeStreptococcus pneumoniae Haemophilus influenzaeHaemophilus influenzae Moraxella catarrhalisMoraxella catarrhalis Streptococcus pyogenesStreptococcus pyogenes Staphylococcus aureusStaphylococcus aureus Gram-negative pathogensGram-negative pathogens Group B streptococci and gram-negative bacilliGroup B streptococci and gram-negative bacilli

ACUTE OTITIS MEDIAACUTE OTITIS MEDIA

Rupture of the eardrum Bulging and thickening of the tympanic membrane

Normal right tympanic membrane and middle ear

Bulging right tympanic membrane in acute otitis media

Diagnostic Workup

• Audiogram and CT scan• Culture from otorrhea • Typanocentesis, removal of fluid behind the eardrum

Treatment OptionsTreatment Options

Myringotomy if middle ear is not drainingMyringotomy if middle ear is not draining Addition of steroid therapy to prevent hearing loss and labyrinthitis Addition of steroid therapy to prevent hearing loss and labyrinthitis

ossificans.ossificans.

OTITIS INTERNA OTITIS INTERNA

Epidemiology & Pathogenesis

Other known as Labyrinthitis

Occurs when toxic mediators reach the membranous labyrinth

Incidence is unknown but is uncommon.

• Sudden onset of mild to moderate hearing loss• Occasionally vertigo• Otalgia • Fever, Dizziness, Nausea and Vomitting

Signs and Symptoms

Causative Agents

Streptococcus pneumoniaeStreptococcus pneumoniae Haemophilus influenzaeHaemophilus influenzae Moraxella catarrhalisMoraxella catarrhalis

Diagnostic Workup

• Audiogram and CT scan• Culture from otorrhea • Typanocentesis, removal of fluid behind the eardrum

Treatment OptionsTreatment Options

Myringotomy if middle ear is not drainingMyringotomy if middle ear is not draining Addition of steroid therapy to prevent hearing loss and labyrinthitis Addition of steroid therapy to prevent hearing loss and labyrinthitis

ossificans.ossificans.

Latest Update(SOURCE: Archives of Otolaryngology---Head and Neck, July 2009, Vol.135 #7)

• Title of the Article: Virulence of Pneumococcal Proteins on the Inner Ear

• Investigate the effects of the virulence characteristics of specific pneumococcal proteins on the inner ear.

• Most of the animals inoculated with high dose pneumolysin or wild-type bacteria showed severe pathologic changes of the inner ears. The inner ears of most animals inoculated with surface protein A or surface antigen A-deficient bacteria appeared normal.

• Pneumococcal surface protein A and pneumococcal surafec antigen A are 2 important virulence factors in inner ear damage secondary to pneumococcal otitis media.

• Mutation of these virulence factors results in less inner ear damage.

Infections of the mouth

GROUP 9 3MBGROUP 9 3MBKathleen CedilloKathleen Cedillo

Richelle Grace S. PazzibuganRichelle Grace S. PazzibuganAlane Biffany TanAlane 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

Disease and infection in the Oral Cavity1.Dental carries2.Periodontal disease3.Trench Mouth4.Strep throat5.Ludwig’s angina6.Bacterial Parotitis

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, starch like 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

Work-up

Gram staining: +Gram staining: + BAP, MM10 sucrose, mitis salivarius-bacitracin BAP, MM10 sucrose, mitis salivarius-bacitracin

(MSB) agar(MSB) agar α-hemolysis on BAPα-hemolysis on BAP Resistant to BEA, sodium desoxycholate, and Resistant to BEA, sodium desoxycholate, and

optichinoptichin

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• Sometimes reffered to “pyorrhoea”• 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

Work-up

Gram stain: -Anaerobic BAP (+), Laked kanamycin-vancomycin (LKV)(-)Positive results: spot indoleNegative results: catalase, nitrate reduction, urease, and lipaseResitant to collistin, and kanamycinSusceptible to vancomycin

Treatment and prevention

• Careful flossing and tooth brushing• 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

“STREP THROAT”

Definition & EPIDEMIOLOGY

• Bacterial throat infection that makes your throat itchy and sore.

• Caused by group A Streptococcus (S.pyogenes)• About 15 % - 40 % cases are from children ages 5-15

years old.• 5 % - 10 % are cases from adults.

Signs and Symptoms• Throat pain• Difficulty in swallowing• Red and swollen tonsils• Tiny red spots on the

soft or hard palate• Swollen, tender lymph

glands (nodes) in your neck

Inflammation and red spots caused by the infection

Signs and Symptoms• Fever• Head ache• Rash• Stomach ache• Vomiting

Inflammation and red spots caused by the infection

MODES OF TRANSMISSION

• It can spread through air by droplets.• The infection could also be acquired by

sharing of utensils.• You can also pick up the bacteria from a

doorknob or other surface and transfer them to your nose or mouth

ETIOLOGIC AGENT

• S.pyogenes• Gram positive • Nonmotile• Non-spore forming in

pairs or chains.• Fermentative

metabolism• Catalase negative

Gram stain of S.pyogenes Gram stain of S.pyogenes

ETIOLOGIC AGENT

• Facultative anaerobe• typically have a capsule

composed of hyaluronic acid

• Normally grows on media that contains blood ( SBAP).

S.pyogenes in blood agar shows beta-hemolysis

S.pyogenes in blood agar shows beta-hemolysis

VIRULENCE FACTORS

• M protein, fibronectin-binding protein (Protein F) and lipoteichoic acid for adherence.

• Hyaluronic acid capsule as an immunological disguise and to inhibit phagocytosis.

• M-protein to inhibit phagocytosis.• Invasins such as streptokinase, streptodornase

(DNase B), hyaluronidase, and streptolysins• Exotoxins, such as pyrogenic (erythrogenic) toxin

TESTS & DIAGNOSIS

• Throat culture.- The sample is then

cultured in a laboratory for the presence of bacteria, but results may take as long as two days.

TESTS & DIAGNOSIS

• Rapid antigen test- This test can detect strep bacteria in minutes by

looking for foreign substances (antigens) in the throat.

- If the test confirms positive result for strep bacteria, antibiotic treatment can begin right away

TESTS & DIAGNOSIS

• Rapid DNA test.- Newer rapid tests use DNA technology to

detect strep throat in a day or less from a throat swab

- These tests are as accurate as throat cultures, and the results are available sooner

TREATMENT

• Oral Antibiotics• - Penicillin and cephalosphorin• Pain relievers• -ibuprofen and acetaminophen

Home remedies

• Warm saline solution gargle• Get enough sleep• Eat soothing foods• Use a humidifier• Stay away from irritants

Ludwig’s angina

• By definition, A rapidly spreading, bilateral, indurated cellulitis occurring in the floor of the mouth.

• Result of abscess of the second or third molar teeth with penetration into the submaxillary space before the mylohyoid region and initiation of cellulitis. ( Tschiassny)

• 75-80% of cases were of dental cause followed by penetrating injury of the floor of the mouth, with mandibular fractures accounting for the rest of the cases. (Tschiassny)

• 85% dental pathological reason, 40% extraction of diseased molar (Patterson)

Anatomy & Pathogenesis

• The floor of the mouth is composed of 2 spaces:

1. Sublingual space2. Submandibular space

• The cellulitis usually begins in the submandibular space, resulting from an infected molar.

Anatomy & Pathogenesis

• From the infected molar, the cellulitis rapidly spreads to involve sublingual space, usually on a bilateral basis.

• The mandible and superficial layer of the deep cervical facia presenting relatively unyielding barriers superiorly and laterally, the tongue is forced upward and posteriorly.

• The infection may also spread posteriorly to the carotid sheath or retropharyngeal space or both by crossing the lateral pharyngeal space.

Cause

• Most of the time, cases of Ludwig’s angina are of dental origin.

• Usually develops from dental or periodontal infection, especially of the 2nd and 3rd mandibular molars.

• Problems regarding poor dental hygiene, tooth extraction and trauma may also be associated with the infection.

Signs and symptoms

• Major manifestation:- Toothache- Severe, tender induration of submandibular region- Trismus- Drooling and inability to swallow- Stridor from laryngeal edema- Tongue elevation

• Fever , chills, tachycardia are usually present.

Signs and symptoms

- tongue elevation- Neck rigidity- Fetid breath

May Be present:- Fever, chills, tachycardia

Etiologic agent

• Alpha hemolytic Streptococci• S. aureus• Mixed oral flora• Aerobes• Anaerobes

Alpha hemolytic streptococci

• Gram positive• Spherical or coccoid in chains• No endospores produced• Catalase negative• Produces a zone of greenish discoloration around the

colony In blood agar plate.• Incomplete lysis

Staphylococcus aureus

• Gram positive cocci in cluters• Facultative anerobe• Catalase positive• Coagulase positive• Shows hemolysis on blood agar plates• In Trypticase soy broth, (blood specimen)• Thiogycollate medium( aerobic and anaerobic)• Tryticase soy broth (fastidious)• Phenol red glocose ( yellow, production of acid)

Staphylococcus Aureus in gram stainStaphylococcus Aureus in gram stain

Diagnosis

CRITERIA:

• It must be rapidly progressive cellulitis; not abscess• Must develop along facial planes with direct

extensions; must not involved lymphatic spread.• The tongue must be elevated• Must involve both sublingual and sub maxillary

spaces and is usually bilateral

Laboratory examination

• X-ray• Nasopharyngeal Fiberoptic examination• Panoramic tomography• Tracheostomy

Treatment

Antibiotics• Penicillin G• Clindamycin• Chloramphenicol• Tracheostomy• surgical drainage

Bacterial Parotitis

- Infection of one or both parotid gland.

EPIDEMIOLOGY • Mostly occurs in postoperative patients who are

dehydrated.• Common in elderly patients

Bacterial Parotitis

• Ascending infection from the oral cavity is assumed to be the cause.

Elderly man with parotid abscess

Anatomy

• Parotid gland is the largest of all salivary gland.

• It is found wrapped around the mandibular ramus , and it secretes saliva through Stensen's duct into the oral cavity, to facilitate mastication and swallowing.

Anatomy

• The gland occupies the parotid fascial space, an area posterior to the mandibular ramus, anterior and inferior to the ear.

Signs and symptoms

• Erythema• pain• Swelling• Xerostomia• Difficulty in chewing• Ear ache• Pus formation inside the cheeks

Etiologic Agents

Most common isolate:• Staphylococcus aureus

Recent studies:• Alpha-haemolytic Streptococcus spp. • Haemophilus spp. • Eikenella corrodens • Prevotella spp. • Strictly anaerobic Gram-positive cocci

Etiologic Agents

Less common Pathogens• Enterobacteriaceae • Other Gram-negative bacilli • Anaerobes

* Mostly seen in hospitalized patients with previous antibiotic therapy.

Staphylococcus aureus • Gram positive cocci in cluters• Facultative anaerobe• Catalase positive• Coagulase positive• Shows hemolysis on blood agar plates• In Trypticase soy broth, (blood specimen)• Thioglycollate medium( aerobic and anaerobic)• Tryticase soy broth (fastidious)• Phenol red glucose ( yellow, production of acid)

Staphylococcus Aureus in gram stainStaphylococcus Aureus in gram stain

Diagnosis

• Pus collection - By Fine needle- aspiration on the tail of the gland.

• Parotid Massage fluid- For culture and sensitivity testing

• Swab of the papilla in the parotid glad- located opposite the second upper molar and in parotitis a

bead of pus may be seen emerging from the duct.

Diagnosis

• CT scan / MRI scan- May be used to determine the size, shape, and some qualities

of neoplasms or swelling within the gland.

• Sialography- Used to demonstrate the anatomy of the drainage system

and is a very useful test.

Treatment

ANTIBIOTICS- IV co-amoxiclav - Penicillin / Clidamycin- Vancomycin

SURGERY- Surgical Drainage (stensen duct)- In chronic parotitis, removal of parotid glad after antibiotic

therapy.

Treatment

• Parotid Gland massage- To relief discomfort and to increase blood flow production.

• Warm Salt water rinse- To moisten the mouth

• Taking mint candies

Bacterial Parotitis

Abscess Formation in the gland and ruptures in the skin

Synergistic Use of Ultrasound and Sonic Motion for Removal of Dental Plaque BacteriaPierre D. Mourad , PhD, Frank A. Roberts, DDS, PhD, Christopher McInnes, PhD

In this article, the authors demonstrate the fecundity of a multidisciplinary environment by reviewing their early work that shows that ultrasound could be added to a power toothbrush to enhance removal of dental plaque bacteria. They hypothesized that sonic brush head motion would generate bubbles in a dentifrice so that ultrasound beamed into that slurry would cause those bubbles to expand and contract in a manner that would dislodge the plaque bacteria adherent to the tooth surfaces. Streptococcus mutans bacteria adherent to various surfaces was used as a model of dental plaque on human teeth. Research demonstrated that the combination of sonic and ultrasound processes could synergistically remove S.mutans biofilm. This finding established the proof of concept that eventually led to the development of a power toothbrush that uses both ultrasound and sonic activity.

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