SORE THROAT, EARACHE, AND UPPER - Secondary bacterial infections
31 RESPIRATORY SYMPTOMS
NONSPECIFIC INFECTIONS OF THE UPPER RESPIRATORY
TRACT
Nonspecific URIs
- have no prominent localizing features
- identified by a variety of descriptive names, including:
▪ acute infective rhinitis,
▪ acute rhinopharyngitis/nasopharyngitis,
▪ acute coryza,
▪ acute nasal catarrh,
▪ common cold
ETIOLOGY
Rhinovirus
- most common cause of URI (~30–40% of cases)
Other causes include:
1. Influenza virus (three immunotypes; Chap. 195)
2. Parainfluenza virus (four immunotypes)
3. Coronavirus (at least three immunotypes),
4. Adenovirus (47 immunotypes) (Chap. 194)
Respiratory syncytial virus (RSV)
- a well-established pathogen in pediatric populations;
recognized cause of significant disease in elderly and
immunocompromised individuals
A specific diagnostic workup beyond a clinical diagnosis is
generally unnecessary in an otherwise healthy adult.
CLINICAL MANIFESTATIONS
Signs and symptoms of nonspecific URI
- are similar to those of other URIs but lack a pronounced
localization to one particular anatomic location, such as
the sinuses, pharynx, or lower airway
- commonly presents as an acute, mild, and self-limited
catarrhal syndrome with a median duration of ~1 week
(range, 2–10 days)
- Principal signs and symptoms:
▪ rhinorrhea (with or without purulence),
▪ nasal congestion,
▪ cough,
▪ sore throat
- Other manifestations, such as fever, malaise, sneezing,
lymphadenopathy, and hoarseness, are more variable,
with fever more common among infants and young
children.
- Myalgias and fatigue
▪ sometimes are seen with influenza and
parainfluenza infections
- Conjunctivitis
▪ may suggest infection with adenovirus or
enterovirus
- Findings on physical examination are frequently
nonspecific and unimpressive.
- Between 0.5 and 2% of colds are complicated by
secondary bacterial infections (e.g., rhinosinusitis, otitis
media, and pneumonia), particularly in higher-risk
populations such as infants, elderly persons, and
chronically ill or immunosuppressed individuals.
▪ usually are associated with a prolonged course
of illness, increased severity of illness, and
localization of signs and symptoms, often as a
rebound after initial clinical improvement (the
“double-dip” sign)
▪ Purulent secretions from the nares or throat
o often are misinterpreted as an
indication of bacterial sinusitis or
pharyngitis.
o These secretions, however, can be
seen in nonspecific URI and, in the
absence of other clinical features, are
poor predictors of bacterial infection.
TREATMENT
Nonspecific Upper Respiratory Infections
- Antibiotics have no role in the treatment of
uncomplicated nonspecific URI, and their misuse
facilitates the emergence of antimicrobial resistance;
in healthy volunteers, a single course of a commonly
prescribed antibiotic like azithromycin can result in
macrolide resistance in oral streptococci many
months later.
- In the absence of clinical evidence of bacterial
infection, treatment remains entirely symptom based,
with use of decongestants and nonsteroidal anti-
inflammatory drugs.
- Clinical trials of zinc, vitamin C, echinacea, and other
alternative remedies have revealed no consistent
benefit in the treatment of nonspecific URI.
INFECTIONS OF THE SINUS
Rhinosinusitis
- refers to an inflammatory condition involving the nasal
sinuses
Most cases of sinusitis involve more than one sinus
- the maxillary sinus
▪ is most commonly involved;
- next, in order of frequency, are the
1. ethmoid,
2. frontal, and
3. sphenoid sinuses
- Each sinus is lined with a respiratory epithelium that
produces mucus, which is transported out by ciliary
action through the sinus ostium and into the nasal cavity.
- Normally, mucus does not accumulate in the sinuses,
which remain mostly sterile despite their adjacency to
the bacterium-filled nasal passages.
- Sinus ostia are obstructed or when ciliary clearance is
impaired or absent
▪ the secretions can be retained, producing the
typical signs and symptoms of sinusitis
▪ As these secretions accumulate with
obstruction, they become more susceptible to
infection with a variety of pathogens, including
viruses, bacteria, and, rarely, fungi.
 RHINOSINUSITIS
Acute rhinosinusitis
- defined as sinusitis of <4 weeks’ duration
- constitutes the vast majority of sinusitis cases
- occur primarily as a consequence of a preceding viral
URI
ETIOLOGY
The ostial obstruction in rhinosinusitis can arise from both
infectious and noninfectious causes.
Noninfectious etiologies:
1. allergic rhinitis (with either mucosal edema or polyp
obstruction)
2. barotrauma (e.g., from deep-sea diving or air travel)
3. exposure to chemical irritants
Obstruction can also occur with:
1. nasal and sinus tumors (e.g., squamous cell carcinoma)
2. granulomatous diseases (e.g., granulomatosis with
polyangiitis, rhinoscleroma)
3. conditions leading to altered mucus content (e.g., cystic
fibrosis) can cause sinusitis through impaired mucus
clearance
Nasotracheal intubation and nasogastric tubes
- are major risk factors for nosocomial sinusitis in ICU
Viral rhinosinusitis
- more common than bacterial sinusitis
- the viruses most commonly isolated—both alone and
with bacteria—have been:
▪ rhinovirus,
▪ parainfluenza virus
▪ influenza virus
Bacterial causes of sinusitis
- S. pneumoniae and non-typable Haemophilus
influenzae
▪ are the most common among community
acquired pathogens
▪ accounting for 50–60% of cases
- Moraxella catarrhalis
▪ causes disease in a significant percentage
(20%) of children but a lesser percentage of
adults
- It is difficult to assess whether a cultured bacterium
represents a true infecting organism, an insufficiently
deep sample (which would not be expected to be sterile),
or—especially in the case of previous sinus surgeries—
a colonizing organism.
- Anaerobes
▪ occasionally are found in association with
infections of the roots of premolar teeth that
spread to the adjacent maxillary sinuses
- Nosocomial cases commonly are associated with
bacteria prevalent in the hospital environment, including:
▪ S. aureus
▪ Pseudomonas aeruginosa
▪ Serratia marcescens
▪ Klebsiella pneumoniae
▪ Enterobacter species
- Fungi
▪ also are established causes of sinusitis,
although most acute cases affect
immunocompromised patients and represent
invasive, life-threatening infections
▪ Rhinocerebral mucormycosis
o best known example caused by fungi
of the order Mucorales, which
includes Rhizopus, Rhizomucor,
Mucor, Lichtheimia (formerly
Mycocladus, formerly Absidia), and
Cunninghamella
▪ these infections classically occur in diabetic
patients with ketoacidosis but can also develop
in transplant recipients, patients with
hematologic malignancies, and patients
receiving chronic glucocorticoid or
deferoxamine therapy
▪ Other hyaline molds, such as Aspergillus and
Fusarium species, also are occasional causes
of this disease.
CLINICAL MANIFESTATIONS
Common presenting symptoms of sinusitis:
1. nasal drainage and congestion
2. facial pain or pressure
3. headache
4. Other nonspecific manifestations include:
a. cough,
b. sneezing,
c. fever
Thick, purulent or discolored nasal discharge is often thought to
indicate bacterial sinusitis but also occurs early in viral infections
such as the common cold and is not specific to bacterial infection.
Bacterial sinusitis
- occasionally associated with tooth pain most often
involving the upper molars, as well as halitosis
Acute sinusitis
- sinus pain or pressure often localizes to the involved
sinus (particularly the maxillary sinus) and can be worse
when the patient bends over or is supine.
Manifestations of advanced sphenoid or ethmoid sinus infection
can be profound, including:
1. severe frontal or retroorbital pain radiating to the occiput
2. thrombosis of the cavernous sinus
3. signs of orbital cellulitis.
Acute focal sinusitis
- is uncommon but should be considered with severe
symptoms involving the maxillary sinus and fever,
regardless of illness duration
- This condition is typically associated with red, hot, and
swollen sinuses that are extremely tender to palpation;
- is of staphylococcal etiology;
- requires emergent debridement and initial IV
administration of antibiotic
Advanced frontal sinusitis
- can present with a condition known as Pott’s puffy
tumor, with soft-tissue swelling and pitting edema over
the frontal bone from a communicating subperiosteal
abscess.
Life-threatening complications of sinusitis are rare but include:
1. meningitis
2. epidural abscess
3. cerebral abscess.
Acute fungal rhinosinusitis (such as mucormycosis)
- often present with symptoms related to pressure effects,
particularly when the infection has spread to the orbits
and cavernous sinus
- common signs:
▪ orbital swelling and cellulitis
▪ proptosis
▪ ptosis
▪ decreased extraocular movement
▪ retro- or periorbital pain
- the use of CT or sinus radiography is not recommended
▪ more advanced cases:
for acute disease, particularly early in the course of
o Nasopharyngeal ulcerations,
illness (i.e., at <10 days) in light of the high prevalence
o Epistaxis
of similar findings among patients with acute viral
o headaches are also common,
rhinosinusitis.
o involvement of cranial nerves V and
- In the evaluation of persistent, recurrent, or chronic
VII
sinusitis, CT of the sinuses becomes the radiographic
▪ Bony erosion may be evident on examination or
study of choice.
endoscopy
Sinus CT
Acute nosocomial sinusitis
- should be used in confirming cases of suspected acute
- are often critically ill and thus do not manifest the typical
nosocomial sinusitis should be
clinical features of sinus disease. This diagnosis should
- a sinus aspirate for culture and susceptibility testing
be suspected, however, when hospitalized patients with
should be obtained because therapy should target the
appropriate risk factors (e.g., nasotracheal intubation)
offending organism before the initiation of antimicrobial
develop fever without another apparent cause.
therapy
DIAGNOSIS
TREATMENT
Illness duration
- one clinical feature that has been used to help guide Acute Rhinosinusitis
diagnostic and therapeutic decision-making - Most patients with a clinical diagnosis of acute
Acute bacterial sinusitis rhinosinusitis improve without antibiotic therapy.
- is uncommon in patients whose symptoms have lasted - The preferred initial approach in patients with mild to
<10 days moderate symptoms of short duration is therapy
▪ expert panels now recommend reserving this aimed at symptom relief and facilitation of sinus
diagnosis for patients with “persistent” drainage, such as with:
symptoms (i.e., symptoms lasting >10 days in ▪ oral and topical decongestants
adults or >10–14 days in children) ▪ nasal saline lavage
accompanied by the three cardinal signs of: ▪ nasal glucocorticoids (at least in patients
1. purulent nasal discharge with a history of chronic sinusitis or
2. nasal obstruction, and allergies)
3. facial pain (Table 31-1) - Antibiotic therapy
▪ can be considered for:
1. adult patients whose condition does not
improve after 10–14 days,
2. patients with more severe symptoms
(regardless of duration) should be
treated with antibiotics
- Watchful waiting
▪ remains a viable option in many cases
 - Empirical antibiotic therapy
▪ for community-acquired sinusitis in adults
o should consist of the narrowest-
spectrum agent active against the
most common bacterial pathogens,
including S. pneumoniae and H.
influenzae—e.g.,
amoxicillin/clavulanate (with the
decision guided by local rates of β-
lactamase-producing H. influenzae)
- Sinus aspiration and/or lavage
▪ patients who do not respond to initial
antimicrobial therapy and must be done by
an otolaryngologist
Antibiotic prophylaxis to prevent episodes of recurrent acute
bacterial sinusitis is not recommended.
- Surgical intervention and IV antibiotic
administration
▪ usually are reserved for patients with severe
disease or those with intracranial
complications such as abscess and orbital
involvement
▪ Extensive surgical debridement
treatment with IV antifungal agents active
against fungal hyphal forms, such as
amphotericin B
o required in immunocompromised
patients with acute invasive fungal
sinusitis and
- Treatment of nosocomial sinusitis should begin with
broadspectrum antibiotics to cover common and
often resistant pathogens such as S. aureus and
gram-negative bacilli.
- Therapy then should be tailored to the results of
culture and susceptibility testing of sinus aspirates.
CHRONIC SINUSITIS
Chronic sinusitis
- is characterized by symptoms of sinus inflammation
lasting >12 weeks
- most commonly associated with either bacteria or fungi,
and clinical cure in most cases is very difficult
Chronic bacterial sinusitis
- infection is thought to be due to the impairment of
mucociliary clearance from repeated infections rather
than to persistent bacterial infection
- Patients experience constant nasal congestion and
sinus pressure, with intermittent periods of greater
severity, which may persist for years
- CT
▪ can be helpful in determining the extent of
disease, detecting an underlying anatomic
defect or obstructing process (e.g., a polyp),
and assessing the response to therapy.
- Management should involve an otolaryngologist to
conduct endoscopic examinations and obtain tissue
samples for histologic examination and culture.
- An endoscopy-derived culture not only has a higher
yield but also allows direct visualization for abnormal
anatomy.
Although certain conditions (e.g., cystic fibrosis) can predispose
patients to chronic bacterial sinusitis, most patients with chronic
rhinosinusitis do not have obvious underlying conditions that
result in the obstruction of sinus drainage, the impairment of
ciliary action, or immune dysfunction.
Chronic fungal sinusitis
- is a disease of immunocompetent hosts and is usually
noninvasive, although slowly progressive invasive
disease is sometimes seen
▪ Noninvasive disease
o associated with hyaline molds such as
Aspergillus species and
dematiaceous molds such as
Curvularia or Bipolaris species
- In mild, indolent disease
▪ which usually occurs in the setting of repeated
failures of antibacterial therapy, only
nonspecific mucosal changes may be seen on
sinus CT.
& ▪ Endoscopic surgery is usually curative in these
cases, with no need for antifungal therapy.
- Long-standing
▪ often unilateral symptoms and opacification of
a single sinus on imaging studies as a result of
a mycetoma (fungus ball) within the sinus.
▪ Treatment for this condition also is surgical,
although systemic antifungal therapy may be
warranted in the rare case in which bony
erosion occurs.
Allergic fungal sinusitis
- is seen in patients with a history of nasal polyposis and
asthma, who often have had multiple sinus surgeries
- Patients with this condition produce a thick, eosinophil-
laden mucus with the consistency of peanut butter that
contains sparse fungal hyphae on histologic examination
- These patients often present with pansinusitis
TREATMENT
Chronic Sinusitis
- Treatment can be challenging and consists primarily
of repeated culture-guided courses of antibiotics,
sometimes for 3–4 weeks or longer at a time;
- administration of intranasal glucocorticoids; and
- mechanical irrigation of the sinus with sterile saline
solution
▪ When this management approach fails,
sinus surgery may be indicated and
sometimes provides significant, albeit short-
term, alleviation.
- Surgical removal of impacted mucus
▪ treatment of chronic fungal sinusitis
▪ Recurrence is common.
 INFECTIONS OF EXTERNAL EAR STRUCTURES
AURICULAR CELLULITIS
Auricular cellulitis
- an infection of the skin overlying the external ear and
typically follows minor local trauma but without apparent
involvement of the ear canal or inner structures
- presents as the typical signs and symptoms of:
1. cellulitis, with tenderness,
2. erythema,
3. swelling,
4. warmth of the external ear (particularly the lobule)
- Treatment consists of:
1. warm compresses
2. oral antibiotics such as cephalexin or dicloxacillin
a. that are active against typical skin and soft-
tissue pathogens (specifically, S. aureus
and streptococci)
3. IV antibiotics such as a first-generation
cephalosporin (e.g., cefazolin) or a penicillinase-
resistant penicillin (e.g., nafcillin are needed for
more severe cases, with consideration of MRSA if
either risk factors or failure of therapy point to this
organism.
PERICHONDRITIS
Perichondritis
- an infection of the perichondrium of the auricular
cartilage, typically follows local trauma (e.g., piercings,
burns, or lacerations)
- Chondritis
▪ when the infection spreads down to the
cartilage of the pinna itself
- The infection may closely resemble auricular cellulitis,
with erythema, swelling, and extreme tenderness of the
pinna, although the lobule is less often involved in
perichondritis.
- The most common pathogens are:
▪ P. aeruginosa
▪ S. aureus
- Treatment consists of:
1. systemic antibiotics active against both P.
aeruginosa and S. aureus.
2. antipseudomonal penicillin (e.g., piperacillin) or a
3. combination of a penicillinase-resistant penicillin
and an antipseudomonal quinolone (e.g., nafcillin
plus ciprofloxacin)
4. Incision and drainage may be helpful for culture and
for resolution of infection, which often takes weeks.
When perichondritis fails to respond to adequate antimicrobial
therapy, clinicians should consider a noninfectious inflammatory
etiology such as relapsing polychondritis.
OTITIS EXTERNA
Otitis Externa
- refers to a collection of diseases involving primarily the
auditory meatus
- usually results from a combination of heat and retained
moisture, with desquamation and maceration of the
epithelium of the outer ear canal
- The disease exists in several forms:
1. Localized
2. Diffuse
3. Chronic
4. Invasive
- All forms are predominantly bacterial in origin, with P.
aeruginosa & S. aureus the most common pathogens.
Acute localized otitis externa (furunculosis)
- can develop in the outer third of the ear canal, where
skin overlies cartilage and hair follicles are numerous
- S. aureus
▪ is the usual pathogen
- Treatment
▪ oral antistaphylococcal penicillin (e.g.,
dicloxacillin or cephalexin)
▪ incision and drainage
o in cases of abscess formation
Acute diffuse otitis externa
- is also known as swimmer’s ear
- although it can develop in patients who have not recently
been swimming
- Heat, humidity, and the loss of protective cerumen lead
to excessive moisture and elevation of the pH in the ear
canal, which in turn lead to skin maceration and irritation
- P. aeruginosa
▪ the predominant pathogen
▪ although other bacteria—and rarely yeasts—
have been recovered from patients with this
condition
- The illness often starts with itching and progresses to
severe pain, which is usually elicited by manipulation of
the pinna or tragus.
- The onset of pain is generally accompanied by the
development of an erythematous, swollen ear canal,
often with scant white, clumpy discharge.
- Treatment:
▪ cleansing the canal to remove debris
▪ enhance the activity of topical therapeutic
agents (usually hypertonic saline or mixtures of
alcohol and acetic acid)
▪ Glucocorticoids
o Decreases inflammation by adding to
the treatment regimen or by using
Burow’s solution (aluminum acetate
in water)
▪ Antibiotics are most effective when given
topically.
▪ Otic mixtures provide adequate pathogen
coverage; these preparations usually combine
neomycin with polymyxin, with or without
glucocorticoids.
 ▪ Systemic antimicrobial agents - P. aeruginosa
o typically are reserved for severe ▪ is by far the most common offender, although
disease or infections in S. aureus, Staphylococcus epidermidis,
immunocompromised hosts. Aspergillus, Actinomyces, and some gram-
Chronic otitis externa negative bacteria also have been associated
- is caused primarily by repeated local irritation, most with this disease.
commonly arising from persistent drainage from a - In all cases, the external ear canal should be cleansed
chronic middle-ear infection and a biopsy specimen of the granulation tissue within
- Other causes of repeated irritation, such as insertion of the canal (or of deeper tissues) obtained for culture of
cotton swabs or other foreign objects into the ear canal, the offending organism.
can lead to this condition, as can rare chronic infections - IV antibiotic therapy
such as syphilis, tuberculosis, and leprosy ▪ should be given for a prolonged course (6–8
- Typically presents as erythematous, scaling dermatitis weeks)
in which the predominant symptom is pruritus rather ▪ directed specifically toward the recovered
than pain; this condition must be differentiated from pathogen
several others that produce a similar clinical picture, o For P. aeruginosa
such as: • the regimen typically
▪ atopic dermatitis includes an
▪ seborrheic dermatitis antipseudomonal penicillin
▪ psoriasis or cephalosporin (e.g.,
▪ dermatomycosis piperacillin or cefepime),
- Therapy consists of: sometimes with an
▪ identifying and treating or removing the aminoglycoside or a
offending process fluoroquinolone, the latter of
▪ successful resolution is frequently difficult. which can even be
Invasive otitis externa administered orally given its
- also known as malignant or necrotizing otitis externa excellent bioavailability.
- is an aggressive and potentially life-threatening disease ▪ Antibiotic drops containing an agent active
that occurs predominantly in elderly diabetic patients and against Pseudomonas (e.g., ciprofloxacin) are
other immunocompromised persons usually prescribed and are combined with
- The disease begins in the external canal as a soft-tissue glucocorticoids to reduce inflammation.
infection that progresses slowly over weeks to months ▪ Cases of invasive Pseudomonas otitis externa
and often is difficult to distinguish from a severe case of recognized in the early stages can sometimes
chronic otitis externa because of the presence of be treated with oral and otic fluoroquinolones
purulent otorrhea and an erythematous swollen ear and alone
external canal. ▪ Extensive surgical debridement
- Severe, deep-seated otalgia, frequently out of o once an important component of the
proportion to findings on examination, is often noted and treatment approach, is now rarely
can help differentiate invasive from chronic otitis indicated
externa. Necrotizing otitis externa
- The characteristic finding on examination is granulation - recurrence is documented up to 20% of the time
tissue in the posteroinferior wall of the external canal, - Aggressive glycemic control in diabetics is important not
near the junction of bone and cartilage. only for effective treatment but also for prevention of
- If left unchecked, the infection can migrate to the base recurrence.
of the skull (resulting in skull-base osteomyelitis) and - The role of hyperbaric oxygen has not been clearly
onward to the meninges and brain, with a high mortality established.
rate.
- Cranial nerve involvement INFECTIONS OF MIDDLE-EAR STRUCTURES
▪ is seen occasionally, with the facial nerve Otitis media
usually affected first and most often. - is an inflammatory condition of the middle ear that
- Thrombosis of the sigmoid sinus can occur if the results from dysfunction of the eustachian tube in
infection extends to the area. association with a number of illnesses, including URIs
- CT and chronic rhinosinusitis.
▪ which can reveal osseous erosion of the - The inflammatory response in these conditions leads to
temporal bone and skull base, can be used to the development of a sterile transudate within the
help determine the extent of disease middle-ear and mastoid cavities.
▪ as can gallium and technetium-99 scintigraphy - Infection may occur if bacteria or viruses from the
studies nasopharynx contaminate this fluid, producing an acute
(or sometimes chronic) illness.
 ACUTE OTITIS MEDIA
Acute otitis media
- results when pathogens from the nasopharynx are
introduced into the inflammatory fluid collected in the
middle ear (e.g., by nose blowing during a URI).
- Pathogenic proliferation in this space leads to the
development of the typical signs and symptoms of acute
middle-ear infection.
- The diagnosis of acute otitis media requires the
demonstration of fluid in the middle ear (with tympanic
membrane [TM] immobility) and the accompanying
signs or symptoms of local or systemic illness (Table 31-
2).
TREATMENT
Acute Otitis Media
ETIOLOGY
Acute otitis media
- typically follows a viral URI
- The causative viruses (most commonly RSV, influenza
virus, rhinovirus, and enterovirus) can themselves
cause subsequent acute otitis media;
- more often, they predispose the patient to bacterial otitis
media
- S. pneumoniae
▪ found to be the most important bacterial cause,
isolated in up to 35% of cases
- H. influenzae (nontypable strains) and M. catarrhalis
▪ also are common bacterial causes of acute
otitis media
- Concern is increasing with MRSA as an emerging
etiologic agent.
- Viruses, such as those mentioned above, have been
recovered either alone or with bacteria in 17–40% of
cases.
CLINICAL MANIFESTATIONS
Fluid in the middle ear
- is typically demonstrated or confirmed with pneumatic
otoscopy
- In the absence of fluid
▪ the TM moves visibly with the application of
positive and negative pressure, but this
movement is dampened when fluid is present.
- With bacterial infection
▪ the TM can also be erythematous, bulging, or
retracted and occasionally can perforate
spontaneously.
- The signs and symptoms accompanying infection can be
local or systemic, including
1. Otalgia
2. Otorrhea
3. Diminished hearing
4. Fever
5. Other signs and symptoms occasionally reported
include:
a. Vertigo
b. Nystagmus
c. Tinnitus
- Erythema of the TM
▪ is often evident but is nonspecific as it
frequently is seen in association with
inflammation of the upper respiratory mucosa.
- A higher proportion of treated than untreated patients
are free of illness 3–5 days after diagnosis.
- In the Netherlands, for instance, physicians typically
manage acute otitis media with initial observation,
administering anti-inflammatory agents for
aggressive pain management and reserving
antibiotics for high-risk patients, patients with
complicated disease, or patients whose condition
does not improve after 48–72 h.
- In contrast, many experts in the United States
continue to recommend antibiotic therapy for
children <6 months old in light of the higher
frequency of secondary complications in this young
and functionally immunocompromised population.
- However, observation without antimicrobial therapy is
now the recommended option in the United States for
acute otitis media in children >2 years of age and for
mild to moderate disease without middle-ear
effusion in children 6 months to 2 years of age.
- Treatment is typically indicated for:
▪ patients <6 months old
▪ For children 6 months to 2 years old who
have middle-ear effusion and signs/
symptoms of middle-ear inflammation
▪ for all patients >2 years old who have
bilateral disease, TM perforation,
immunocompromise, or emesis
▪ for any patient who has severe symptoms,
including a fever ≥39°C or moderate to
severe otalgia (Table 31-2).
- Amoxicillin
▪ remains the drug of first choice in
recommendations
- Therapy for uncomplicated acute otitis media typically
is administered for 5–7 days to patients aged ≥6
years; longer courses (e.g., 10 days) should be
reserved for immunocompromised patients or
patients with severe disease, in whom short-course
therapy may be inadequate.
 - A switch in regimen is recommended if there is no
clinical improvement by the third day of therapy,
given the possibility of infection with a β-lactamase-
producing strain of H. influenzae or M. catarrhalis or
with a strain of penicillin-resistant S. pneumoniae.
- Decongestants and antihistamines
▪ are frequently used as adjunctive agents to
reduce congestion and relieve obstruction of
the eustachian tube
RECURRENT ACUTE OTITIS MEDIA
Recurrent acute otitis media
- >3 episodes within 6 months or 4 episodes within 12
months
- is due to relapse or reinfection, although data indicate
that the majority of early recurrences are new infections.
- In general, the same pathogens responsible for acute
otitis media cause recurrent disease
- Recommended treatment
▪ consists of antibiotics active against β-
lactamase-producing organisms
▪ Antibiotic prophylaxis (e.g., with amoxicillin)
can reduce recurrences in patients with
recurrent acute otitis media by an average of
one episode per year
SEROUS OTITIS MEDIA
Serous otitis media (otitis media with effusion)
- fluid is present in the middle ear for an extended period
in the absence of signs and symptoms of infection
- Acute effusions are self-limited; most resolve in 2–4
weeks
- In some cases, however (in particular after an episode
of acute otitis media), effusions can persist for months.
- These chronic effusions are often associated with
significant hearing loss in the affected ear.
- The great majority of cases of otitis media with effusion
resolve spontaneously within 3 months without
antibiotic therapy.
- Antibiotic therapy or myringotomy with insertion of
tympanostomy tubes
▪ typically is reserved for patients in whom
bilateral effusion
1. has persisted for at least 3 months
2. is associated with significant bilateral
hearing loss
CHRONIC OTITIS MEDIA
Chronic suppurative otitis media
- is characterized by persistent or recurrent purulent
otorrhea in the setting of TM perforation
- there is also some degree of conductive hearing loss.
- This condition can be categorized as active or inactive.
▪ Inactive disease
o is characterized by a central
perforation of the TM, which allows
drainage of purulent fluid from the
middle ear.
o When the perforation is more
peripheral, squamous epithelium from
the auditory canal may invade the
middle ear through the perforation,
forming a mass of keratinaceous
debris (cholesteatoma) at the site of
invasion.
o This mass can enlarge and has the
potential to erode bone and promote
further infection, which can lead to
meningitis, brain abscess, or paralysis
of cranial nerve VII
- Treatment of chronic active otitis media is surgical;
mastoidectomy, myringoplasty, and tympanoplasty can
be performed as outpatient surgical procedures, with an
overall success rate of ~80%.
- Chronic inactive otitis media is more difficult to cure,
usually requiring repeated courses of topical antibiotic
drops during periods of drainage.
- Systemic antibiotics may offer better cure rates, but
their role in the treatment of this condition remains
unclear.
MASTOIDITIS
Acute mastoiditis
- was relatively common among children before the
introduction of antibiotics
- Because the mastoid air cells connect with the middle
ear, the process of fluid collection and infection is usually
the same in the mastoid as in the middle ear
- In typical acute mastoiditis
▪ purulent exudate collects in the mastoid air
cells (Fig. 31-1) producing pressure that may
result in erosion of the surrounding bone and
formation of abscess-like cavities that are
usually evident on CT.
▪ Patients typically present with pain, erythema,
and swelling of the mastoid process along
with displacement of the pinna, usually in
conjunction with the typical signs and
symptoms of acute middle-ear infection.
 ▪ Rarely, patients can develop severe
complications if the infection tracks under the
periosteum of the temporal bone to cause a
subperiosteal abscess, erodes through the
mastoid tip to cause a deep neck abscess, or
extends posteriorly to cause septic thrombosis
of the lateral sinus.
- Purulent fluid should be cultured whenever possible to
help guide antimicrobial therapy.
▪ Initial empirical therapy usually is directed
against the typical organisms associated with
acute otitis media, such as S. pneumoniae, H.
influenzae, and M. catarrhalis.
▪ Patients with more severe or prolonged
courses of illness should be treated for
infection with S. aureus and gram-negative
bacilli (including Pseudomonas).
▪ Broad-spectrum empirical therapy should be
narrowed once culture results become
available.
▪ Most patients can be treated conservatively
with IV antibiotics
- Surgery (cortical mastoidectomy)
▪ is reserved for complicated cases and those in
which conservative treatment has failed
INFECTIONS OF THE PHARYNX AND ORAL CAVITY
- Oropharyngeal infections range from mild, self-limited
viral illnesses to serious, life-threatening bacterial
infections.
- Sore throat
▪ The most common presenting symptom
▪ one of the most common reasons for
ambulatory care visits by both adults and
children
ACUTE PHARYNGITIS
Group A β-hemolytic Streptococcus (S. pyogenes)
- the most important source of concern of infection
- is associated with acute glomerulonephritis and acute
rheumatic fever
Penicillin therapy
- reduces the risk of rheumatic fever
ETIOLOGY
Respiratory viruses
- are the most common identifiable cause of acute
pharyngitis
▪ rhinoviruses and coronaviruses
o accounting for large proportions of
cases (~20% and at least 5%,
respectively)
▪ Influenza virus, parainfluenza virus, and
adenovirus
o also account for a measurable share
of cases, with the former two more
seasonal and the latter as part of the
more clinically severe syndrome of
pharyngoconjunctival fever
▪ Herpes simplex virus (HSV) types 1 and 2,
coxsackievirus A, cytomegalovirus (CMV),
and Epstein-Barr virus (EBV)
o other important but less common viral
causes
▪ Acute HIV infection
o can present as acute pharyngitis and
should always be considered in at-risk
populations
Acute bacterial pharyngitis
- is typically caused by S. pyogenes
▪ which accounts for ~5–15% of all cases of acute
pharyngitis in adults; rates vary with the season
and with utilization of the health care system.
Group A streptococcal pharyngitis
- is primarily a disease of children aged 5–15 years;
- it is uncommon among children <3 years old, as is
rheumatic fever
Streptococci of groups C and G
- account for a minority of cases, although these
serogroups are nonrheumatogenic.
Fusobacterium necrophorum
- has been increasingly recognized as a cause of
pharyngitis in adolescents and young adults and, when
sought, is isolated nearly as often as group A
streptococci.
- This organism is important because of the rare but life-
threatening Lemierre disease, which is generally
associated with F. necrophorum and is usually preceded
by pharyngitis
- The remaining bacterial causes of acute pharyngitis are
seen infrequently (<1% of cases each) but should be
considered in appropriate exposure groups because of
the severity of illness if left untreated; these etiologic
agents include:
▪ Neisseria gonorrhoeae
▪ Corynebacterium diphtheriae
▪ Corynebacterium ulcerans
▪ Yersinia enterocolitica
▪ Treponema pallidum (in secondary syphilis)
- Anaerobic bacteria
▪ also can cause acute pharyngitis (Vincent
angina) and can contribute to more serious
polymicrobial infections, such as peritonsillar
or retropharyngeal abscesses
- Atypical organisms: M. pneumoniae and C. pneumoniae
▪ have been recovered from patients with acute
pharyngitis
CLINICAL MANIFESTATIONS
Signs and symptoms accompanying acute pharyngitis are not
reliable predictors of the etiologic agent, the clinical presentation
occasionally suggests one etiology over another.
Acute pharyngitis due to respiratory viruses
- such as rhinovirus or coronavirus usually is not severe
- typically is associated with a constellation of coryzal
symptoms better characterized as nonspecific URI.
 - Findings on physical examination are uncommon; fever
is rare, and tender cervical adenopathy and pharyngeal
exudates are not seen.
Acute pharyngitis from influenza virus
- can be severe and is much more likely to be associated
with fever as well as with myalgias, headache, and
cough.
- The presentation of pharyngoconjunctival fever due to
adenovirus infection is similar.
- Since pharyngeal exudate may be present on
examination, this condition can be difficult to
differentiate from streptococcal pharyngitis.
- However, adenoviral pharyngitis is distinguished by the
presence of conjunctivitis in one-third to one-half of
patients.
Acute pharyngitis from primary HSV infection
- can also mimic streptococcal pharyngitis in some cases,
with pharyngeal inflammation and exudate, but the
presence of vesicles and shallow ulcers on the palate can
help differentiate the two diseases.
- This HSV syndrome is distinct from pharyngitis caused
by coxsackievirus (herpangina), which is associated
with small vesicles that develop on the soft palate and
uvula and then rupture to form shallow white ulcers.
- Acute pharyngitis coupled with fever, fatigue,
generalized lymphadenopathy, and (on occasion)
splenomegaly is characteristic of infectious
mononucleosis due to EBV or CMV.
Acute primary infection with HIV
- is frequently associated with fever and acute pharyngitis
as well as with myalgias, arthralgias, malaise, and
occasionally a nonpruritic maculopapular rash, which
may be followed by lymphadenopathy and mucosal
ulcerations without exudate.
Acute pharyngitis caused by streptococci of groups A, C, and G
- clinical manifestations are similar, ranging from a
relatively mild illness without many accompanying
symptoms to clinically severe cases with profound
pharyngeal pain, fever, chills, and abdominal pain.
- A hyperemic pharyngeal membrane with tonsillar
hypertrophy and exudate is usually seen, along with
tender anterior cervical adenopathy.
- Coryzal manifestations, including cough, are typically
absent; when present, they suggest a viral etiology.
- Strains of S. pyogenes that generate erythrogenic toxin
▪ can also produce scarlet fever characterized by
an erythematous rash and strawberry tongue.
- The other types of acute bacterial pharyngitis (e.g.,
gonococcal, diphtherial, and yersinial) often present as
exudative pharyngitis with or without other clinical
features.
DIAGNOSIS
The primary goal of diagnostic testing is to separate acute
streptococcal pharyngitis from pharyngitis of other etiologies
(particularly viral) so that antibiotics can be prescribed more
efficiently for patients in whom they may be beneficial.
Throat swab culture
- is generally regarded as the most appropriate but cannot
distinguish between infection and colonization and
requires 24–48 h to yield results that vary with technique
and culture conditions.
Rapid antigen-detection tests
- offer good specificity (>90%) but lower sensitivity when
implemented in routine practice.
- Sensitivity has also been shown to vary across the
clinical spectrum of disease (65–90%).
- Several clinical prediction systems (Fig. 31-2) can
increase the sensitivity of rapid antigen-detection tests
to >90% in controlled settings. Since the sensitivities
achieved in routine clinical practice are often lower,
several medical and professional societies continue to
recommend that all negative rapid antigen-detection
tests in children be confirmed by a throat culture to limit
transmission and complications of illness caused by
group A streptococci.
- Cultures and rapid diagnostic tests for other causes of
acute pharyngitis, such as influenza virus, adenovirus,
HSV, EBV, CMV, and M. pneumoniae, are available in
many locations and can be used when these pathogens
are suspected.
- The diagnosis of acute EBV infection depends primarily
on the detection of antibodies to the virus with a
heterophile agglutination assay (monospot slide test)
or enzyme-linked immunosorbent assay.
- Testing for HIV, ideally through a combination
antigen/antibody method, should be performed when
acute primary HIV infection is suspected.
- If other bacterial causes are suspected (particularly N.
gonorrhoeae, C. diphtheriae, or Y. enterocolitica),
specific cultures should be requested since these
organisms may be missed on routine throat swab
culture.
TREATMENT
Pharyngitis
- Antibiotic treatment of pharyngitis due to S. pyogenes
confers numerous benefits, including a decrease in
the risk of rheumatic fever—the primary focus of
treatment.
- When therapy is started within 48 h of illness onset,
symptom duration is decreased modestly.
- An additional benefit of therapy is the potential to
reduce the transmission of streptococcal
pharyngitis, particularly in areas of overcrowding or
close contact.
- Antibiotics should be given in routine cases only
when another bacterial cause has been identified.
- Effective therapy for streptococcal pharyngitis
consists of either a single dose of IM benzathine
penicillin or a full 10-day course of oral penicillin.
- Azithromycin can be used in place of penicillin
- Broader-spectrum (and often more expensive)
antibiotics
▪ also are active against streptococci but offer
no greater efficacy than the agents
mentioned above
- There is no evidence to support antibiotic treatment
of group C or G streptococcal pharyngitis or
pharyngitis in which mycoplasmas or chlamydiae
have been recovered.
- Cultures can be of benefit because F. necrophorum,
an increasingly common cause of bacterial
pharyngitis in young adults, is not covered by
macrolide therapy.
- Long-term penicillin prophylaxis (benzathine
penicillin G, 1.2 million units IM every 3–4 weeks; or
penicillin VK, 250 mg PO twice daily)
▪ is indicated for patients at risk of recurrent
rheumatic fever in order to prevent what
could be catastrophic sequelae of recurrent
streptococcal pharyngitis
- Treatment of viral pharyngitis
▪ is entirely symptom-based except in
infection with influenza virus or HSV.
o For influenza
• the armamentarium
includes the
adamantanes
amantadine and
rimantadine and the
neuraminidase inhibitors
oseltamivir and
zanamivir.
• Administration of all these
agents needs to be
started within 48 h of
symptom onset to reduce
illness duration
meaningfully.
• Among these agents, only
oseltamivir and
zanamivir are active
against both influenza A
and influenza B and
therefore can be used
when local patterns of
infection and antiviral
resistance are unknown.
▪ Oropharyngeal HSV infection
o sometimes responds to treatment
with antiviral agents such as
acyclovir, although these drugs are
often reserved for
immunosuppressed patients.
COMPLICATIONS
Rheumatic fever
- is the best-known complication of acute streptococcal
pharyngitis
- the risk of its following acute infection remains quite low.
- Other complications include:
▪ acute glomerulonephritis and
▪ numerous suppurative conditions such as:
o peritonsillar abscess (quinsy),
o otitis media,
o mastoiditis,
o sinusitis,
o bacteremia, and
o pneumonia
- Although antibiotic treatment of acute streptococcal
pharyngitis can prevent the development of rheumatic
fever, there is no evidence that it can prevent acute
glomerulonephritis.
- Some evidence supports antibiotic use to prevent the
suppurative complications of streptococcal pharyngitis,
particularly peritonsillar abscess, which can also involve
oral anaerobes such as Fusobacterium.
- Abscesses
▪ usually are accompanied by severe pharyngeal
pain, dysphagia, fever, and dehydration;
▪ in addition, medial displacement of the tonsil
and lateral displacement of the uvula are often
evident on examination.
- Early use of IV antibiotics (e.g., clindamycin, penicillin G
with metronidazole)
▪ may eliminate the need for surgical drainage in
some cases
▪ treatment typically involves needle aspiration
or incision and drainage
ORAL INFECTIONS
HSV or Candida species
- most commonly involved in infections of the oral cavity
- In addition to causing painful cold sores on the lips, HSV
can infect the tongue and buccal mucosa, causing the
formation of irritating vesicles.
- Topical antiviral agents (e.g., acyclovir and penciclovir)
▪ can be used externally for cold sores, with
possible benefit, oral or IV acyclovir is often
needed for primary infections, extensive oral
 infections, and infections in
immunocompromised patients.
- Oropharyngeal candidiasis (thrush)
▪ is caused by a variety of Candida species, most
often C. albicans.
▪ Thrush occurs predominantly in neonates,
immunocompromised patients (especially
those with AIDS), and recipients of prolonged
antibiotic or glucocorticoid therapy.
▪ In addition to sore throat, patients often report
a burning tongue or abnormal taste, and
physical examination reveals friable white or
gray plaques on the gingiva, tongue, and oral
mucosa, often with underlying erythema.
▪ Treatment, which usually consists of topical
antifungal (nystatin or clotrimazole) or oral
fluconazole, is typically successful.
▪ In the uncommon cases of fluconazole-
refractory thrush that are seen in some patients
with HIV/AIDS or in patients with resistant
organisms that can sometimes complicate the
treatment of recurrent oral candidiasis, other
therapeutic options include oral voriconazole,
an IV echinocandin (caspofungin, micafungin,
or anidulafungin), or amphotericin B
deoxycholate, if needed.
▪ In these cases, therapy based on culture and
susceptibility test results is ideal.
Vincent angina / Acute necrotizing ulcerative gingivitis / Trench
mouth
- is a unique and dramatic form of gingivitis characterized
by painful, inflamed gingiva with ulcerations of the
interdental papillae that bleed easily.
- Oral anaerobes
▪ are the cause
▪ patients typically have halitosis and frequently
present with fever, malaise, and
lymphadenopathy
- Treatment consists of debridement and oral
administration of penicillin plus metronidazole, with
clindamycin or doxycycline alone as an alternative.
Ludwig angina
- is a rapidly progressive, potentially fulminant form of
cellulitis that involves the bilateral sublingual and
submandibular spaces and that typically originates from
an infected or recently extracted tooth, most commonly
a lower second or third molar. I
- mproved dental care has reduced the incidence of this
disorder substantially.
- Infection in these areas leads to dysphagia,
odynophagia, and “woody” edema in the sublingual
region, forcing the tongue up and back with the potential
for airway obstruction.
- Fever, dysarthria, and drooling also may occur, and
patients may speak in a “hot potato” voice.
- Intubation or tracheostomy may be necessary to secure
the airway, as asphyxiation is the most common cause
of death.
- Patients should be admitted to the hospital and closely
monitored during treatment with IV antibiotics directed
against streptococci and oral anaerobes.
- Recommended agents include ampicillin/sulbactam,
clindamycin, or high-dose penicillin plus
metronidazole.
Septic thrombophlebitis of the internal jugular vein (Lemierre
disease)
- is a rare anaerobic oropharyngeal infection caused
predominantly by F. necrophorum.
- The illness typically starts as a sore throat (most
commonly in adolescents and young adults), which may
present as exudative tonsillitis or peritonsillar abscess.
- Infection of the deep pharyngeal tissue allows organisms
to drain into the lateral pharyngeal space, which contains
the carotid artery and internal jugular vein.
- can result, with associated pain, dysphagia, and
unilateral neck swelling and stiffness.
- Sepsis usually occurs 3–10 days after the onset of sore
throat and is often coupled with metastatic infection to
the lung and other distant sites, with pulmonary abscess
or empyema.
- Occasionally, the infection can extend along the carotid
sheath and into the posterior mediastinum, resulting in
mediastinitis, or it can erode into the carotid artery, with
the early sign of repeated small bleeds into the mouth.
- Treatment consists of IV antibiotics (clindamycin or
ampicillin/sulbactam) and surgical drainage of any
purulent collections.
INFECTIONS OF THE LARYNX AND EPIGLOTTIS
LARYNGITIS
Laryngitis
- is defined as any inflammatory process involving the
larynx and can be caused by a variety of infectious and
noninfectious processes.
- Acute laryngitis
▪ is a common syndrome caused predominantly
by the same viruses responsible for many other
URIs.
▪ most cases of acute laryngitis occur in the
setting of a viral URI
ETIOLOGY
Nearly all major respiratory viruses have been implicated in acute
viral laryngitis, including rhinovirus, influenza virus, parainfluenza
virus, adenovirus, coxsackievirus, coronavirus, and RSV.
Acute laryngitis can also be associated with acute bacterial
respiratory infections such as those caused by group A
Streptococcus or C. diphtheriae (although diphtheria has been
virtually eliminated in the United States).
Another bacterial pathogen thought to play a role (albeit unclear)
in the pathogenesis of acute laryngitis is M. catarrhalis, which
has been recovered from nasopharyngeal cultures in a significant
percentage of cases.
Chronic laryngitis of infectious etiology
- is much less common in developed than in developing
countries.
Laryngitis due to Mycobacterium tuberculosis
- is often difficult to distinguish from laryngeal cancer, in
part because of the frequent absence of signs,
symptoms, and radiographic findings typical of
pulmonary disease.
Histoplasma and Blastomyces
- may cause laryngitis, often as a complication of systemic
infection.
Candida species
- can cause laryngitis as well, often in association with
thrush or esophagitis and particularly in
immunosuppressed patients.
Rare cases of chronic laryngitis are due to Coccidioides and
Cryptococcus.
CLINICAL MANIFESTATIONS
Characeterized by:
- hoarseness
- also can be associated with reduced vocal pitch or
aphonia.
Acute laryngitis
- is caused primarily by respiratory viruses, these
symptoms usually occur in association with other
symptoms and signs of URI, including rhinorrhea, nasal
congestion, cough, and sore throat.
Direct laryngoscopy
- often reveals diffuse laryngeal erythema and edema,
along with vascular engorgement of the vocal folds.
- In addition, chronic disease (e.g., tuberculous
laryngitis) often includes mucosal nodules and
ulcerations visible on laryngoscopy; these lesions are
sometimes mistaken for laryngeal cancer.
TREATMENT
Laryngitis
- is usually treated with humidification and voice rest
alone.
- Antibiotics are not recommended except when group
A Streptococcus is cultured, in which case penicillin
is the drug of choice.
- The choice of therapy for chronic laryngitis depends
on the pathogen, whose identification usually requires
biopsy with culture.
- Patients with laryngeal tuberculosis are highly
contagious because of the large number of organisms
that are easily aerosolized.
▪ These patients should be managed in the
same way as patients with active pulmonary
disease.
CROUP
- denotes a group of diseases collectively referred to as
“croup syndrome,” all of which are acute and
predominantly viral respiratory illnesses characterized by
marked swelling of the subglottic region of the larynx.
- primarily affects children <6 years old. For a detailed
discussion of this entity, the reader should consult a
textbook of pediatric medicine.
EPIGLOTTITIS
Acute epiglottitis (supraglottitis)
- is an acute, rapidly progressive form of cellulitis of the
epiglottis and adjacent structures that can result in
complete—and potentially fatal—airway obstruction in
both children and adults.
- Before the widespread use of H. influenzae type b (Hib)
vaccine, this entity was much more common among
children, with a peak incidence at ~3.5 years of age.
- Mass vaccination against Hib
▪ has reduced the annual incidence of acute
epiglottitis in children by >90%
- Because of the danger of airway obstruction, acute
epiglottitis constitutes a medical emergency, particularly
in children, and prompt diagnosis and airway protection
are of the utmost importance.
ETIOLOGY
Group A Streptococcus
- Most common bacterial pathogens associated with
epiglottitis
- Other pathogens—seen less frequently— include S.
pneumoniae, Haemophilus parainfluenzae, and S.
aureus (including MRSA).
Viruses have not been established as causes of acute epiglottitis.
CLINICAL MANIFESTATIONS AND DIAGNOSIS
Epiglottitis
- typically presents more acutely in young children than in
adolescents or adults.
- On presentation, most children have had symptoms for
<24 h, including high fever, severe sore throat,
tachycardia, systemic toxicity, and (in many cases)
drooling while sitting forward.
- Symptoms and signs of respiratory obstruction also may
be present and may progress rapidly.
- The somewhat milder illness in adolescents and adults
often follows 1–2 days of severe sore throat and is
commonly accompanied by dyspnea, drooling, and
stridor.
- Physical examination of patients with acute epiglottitis
may reveal moderate or severe respiratory distress,
with inspiratory stridor and retractions of the chest
wall.
▪ These findings diminish as the disease
progresses and the patient tires.
- Oropharyngeal examination
▪ reveals infection that is much less severe than
would be predicted from the symptoms—a
finding that should alert the clinician to a cause
 of symptoms and obstruction that lies beyond
the tonsils. T
- he diagnosis often is made on clinical grounds, although
direct fiberoptic laryngoscopy is frequently performed
in a controlled environment (e.g., an operating room) to
visualize and culture the typical edematous “cherry-red”
epiglottis and facilitate placement of an endotracheal
tube.
- Direct visualization in an examination room (i.e., with a
tongue blade and indirect laryngoscopy) is not
recommended because of the risk of immediate
laryngospasm and complete airway obstruction.
- Lateral neck radiographs and laboratory tests
▪ can assist in the diagnosis but may delay the
critical securing of the airway and cause the
patient to be moved or repositioned more than
is necessary, thereby increasing the risk of
further airway compromise.
▪ Neck radiographs
o typically reveal an enlarged
edematous epiglottis (the “thumbprint
sign,” Fig. 31-3), usually with a dilated
hypopharynx and normal subglottic
structures
▪ Laboratory tests
o characteristically document mild to
moderate leukocytosis with a
predominance of neutrophils. Blood
cultures are positive in a significant
proportion of cases.
TREATMENT
Epiglottitis
Security of the airway
- is always of primary concern in acute epiglottitis,
even if the diagnosis is only suspected.
- Once the airway has been secured and specimens of
blood and epiglottis tissue have been obtained for
culture, treatment with IV antibiotics should be given
to cover the most likely organisms, particularly H.
influenzae.
- β-lactam/β-lactamase inhibitor combination or a
third-generation cephalosporin
▪ is recommended
- Ampicillin/sulbactam, cefotaxime, or ceftriaxone is
given, with clindamycin and trimethoprim-
sulfamethoxazole
▪ reserved for patients allergic to β-lactams.
- Antibiotic therapy should be continued for 7–10 days
and should be tailored to the organism recovered in
culture.
- If the household contacts of a patient with H.
influenzae epiglottitis include an unvaccinated child
aged <4 years, all members of the household
(including the patient) should receive prophylactic
rifampin for 4 days to eradicate carriage of H.
influenzae.
INFECTIONS OF DEEP NECK STRUCTURES
Deep neck infections
- are usually extensions of infection from other primary
sites, most often within the pharynx or oral cavity.
- Many of these infections are life-threatening but are
difficult to detect at early stages, when they may be more
easily managed.
- Three of the most clinically relevant spaces in the neck
are the:
1. submandibular (and sublingual) space,
2. the lateral pharyngeal (or parapharyngeal) space,
3. the retropharyngeal space
▪ These spaces communicate with one another
and with other important structures in the head,
neck, and thorax, providing pathogens with
easy access to areas that include the
mediastinum, carotid sheath, skull base, and
meninges.
▪ Once infection reaches these sensitive areas,
mortality rates can be as high as 20–50%.
Infection of the submandibular and/or sublingual space
- typically originates from an infected or recently extracted
lower tooth.
- The result is the severe, life-threatening infection
referred to as Ludwig angina
Infection of the lateral pharyngeal (or parapharyngeal) space
- is most often a complication of common infections of the
oral cavity and upper respiratory tract, including
tonsillitis, peritonsillar abscess, pharyngitis, mastoiditis,
and periodontal infection.
- This space, situated deep in the lateral wall of the
pharynx, contains a number of sensitive structures,
including the carotid artery, internal jugular vein, cervical
sympathetic chain, and portions of cranial nerves IX
through XII; at its distal end, it opens into the posterior
mediastinum.
- Involvement of this space with infection can therefore be
rapidly fatal.
- Examination may reveal some tonsillar displacement,
trismus, and neck rigidity, but swelling of the lateral
pharyngeal wall can easily be missed.
- The diagnosis can be confirmed by CT.
- Treatment consists of airway management, operative
drainage of fluid collections, and at least 10 days of IV
 therapy with an antibiotic active against streptococci
and oral anaerobes (e.g., ampicillin/sulbactam).
- Postanginal septicemia, Lemierre disease
▪ A particularly severe form of this infection
involving the components of the carotid sheath)
Infection of the retropharyngeal space
- also can be extremely dangerous, as this space runs
posterior to the pharynx from the skull base to the
superior mediastinum.
- Infections in this space are more common among
children <5 years old because of the presence of several
small retropharyngeal lymph nodes that typically atrophy
by age 4 years.
- Infection is usually a consequence of extension from
another site of infection—most commonly, acute
pharyngitis.
- Other sources include otitis media, tonsillitis, dental
infections, Ludwig angina, and anterior extension of
vertebral osteomyelitis.
Retropharyngeal space infection
- also, can follow penetrating trauma to the posterior
pharynx (e.g., from an endoscopic procedure).
- Infections are commonly polymicrobial, involving a
mixture of aerobes and anaerobes; group A β-hemolytic
streptococci and S. aureus are the most common
pathogens.
- M. tuberculosis was a common cause in the past but
now is rarely involved in the United States.
Patients with retropharyngeal abscess
- typically present with sore throat, fever, dysphagia, and
neck pain and are often drooling because of difficulty and
pain with swallowing.
- Examination may reveal tender cervical adenopathy,
neck swelling, and diffuse erythema and edema of the
posterior pharynx as well as a bulge in the posterior
pharyngeal wall that may not be obvious on routine
inspection.
- A soft-tissue mass is usually demonstrable by lateral
neck radiography or CT. B
- ecause of the risk of airway obstruction, treatment
begins with securing of the airway, which is followed by
a combination of surgical drainage and IV antibiotic
administration.
- Initial empirical therapy should cover streptococci, oral
anaerobes, and S. aureus; ampicillin/sulbactam,
clindamycin plus ceftriaxone, or meropenem is usually
effective.
- Complications result primarily from extension to other
areas (e.g., rupture into the posterior pharynx may lead
to aspiration pneumonia and empyema).
- Extension may also occur to the lateral pharyngeal
space and mediastinum, resulting in mediastinitis and
pericarditis, or into nearby major blood vessels.

All these events are associated with a high mortality rate.