Pharyngitis

• ETIOLOGY
• Many infectious agents can cause pharyngitis.
• Group A streptococci (Streptococcus pyogenes) are gram-positive,
nonmotile cocci that are facultative anaerobes.
• On sheep blood agar, the colonies are small (1 to 2 mm in
diameter) and have a surrounding zone of beta (clear) hemolysis.
• Other bacterial organisms less often associated with pharyngitis
include group C beta-hemolytic streptococcus; Arcanobacterium
haemolyticum, which is a hemolytic, gram-positive rod; and
Francisella tularensis, the gram-negative coccobacillus that is the
cause of tularemia.
• Chlamydophila pneumoniae, strain TWAR, is
associated with lower respiratory disease, but
also causes sore throat.
• M. pneumoniae is associated with atypical
pneumonia, but also can cause mild
pharyngitis without distinguishing clinical
manifestations.
• Other bacteria, including S. aureus, Hib, and S.
pneumoniae are cultured frequently from the
throats of children with pharyngitis, but their
role in causing pharyngitis is unclear.
• Many viruses cause acute pharyngitis including:
 Adenoviruses(most common)
 rhinoviruses,
 EBV (mononucleosis),
 enteroviruses,
 HIV
• Some viruses, such as adenoviruses, are more likely than
others to cause pharyngitis as a prominent symptom,
whereas other viruses, such as rhinoviruses, are more likely
to cause pharyngitis as a minor part of an illness that
primarily features other symptoms, such as rhinorrhea or
cough.
• EBV (mononucleosis), enteroviruses (herpangina), and
primary HIV infection also produce pharyngitis.
 EPIDEMIOLOGY
• Infections of the upper respiratory tract account for a substantial
proportion of illnesses in children.
• Sore throat is the primary symptom in approximately one third of
such illnesses.
Streptococcal pharyngitis is relatively uncommon before 2 to 3 years
of age, but the incidence increases in young school-age children,
then declines in late adolescence and adulthood.
• Streptococcal pharyngitis occurs throughout the year in temperate
climates, with a peak during the winter and spring.
• The illness often spreads to siblings and classmates.
• Viral infections generally spread via close contact with an infected
person and peak during winter and spring.
 CLINICAL MANIFESTATIONS
 The inflammation of pharyngitis causes:
o cough,
o sore throat,
o dysphagia,
o and fever.
• If involvement of the tonsils is prominent, the
term tonsillitis or tonsillopharyngitis is often
used.
 The onset of streptococcal pharyngitis is often rapid
and associated with:
 prominent sore throat
 moderate to high fever.
 Headache,
 nausea, vomiting, and abdominal pain are frequent.
 In a typical, florid case, the pharynx is distinctly red, and the
tonsils are enlarged and covered with a yellow, blood-tinged
exudate.
 There may be petechiae or "doughnut-shaped" lesions on the
soft palate and posterior pharynx,
 and the uvula may be red, stippled, and swollen.
 The anterior cervical lymph nodes are enlarged and tender to
touch.
• The clinical spectrum of disease is broad,
however, and many children present with only
mild pharyngeal erythema without tonsillar
exudate or cervical lymphadenitis.
• In addition to sore throat and fever, some
patients exhibit the stigmata of scarlet fever:
 circumoral pallor,
 strawberry tongue,
 and a fine diffuse erythematous macular-
papular rash that has the feeling of goose flesh.
• The tongue initially has a white coating, but red and edematous
lingual papillae later project through this coating, producing a
white strawberry tongue.
• When the white coating peels off, the resulting red strawberry
tongue is a beefy red tongue with prominent papillae.
• Compared with classic streptococcal pharyngitis, the onset of
viral pharyngitis is typically more gradual, and symptoms more
often include:
 rhinorrhea,
 cough,
 and diarrhea.
• Many illnesses fall in the general category of upper respiratory
tract infection, in which the symptoms of rhinorrhea and nasal
obstruction are prominent, and systemic symptoms and signs,
such as myalgia and fever, are absent or mild.
Gingivostomatitis
• is characteristic of HSV-1 and usually occurs in children 1 to 5 years old, with the
highest incidence from 9 to 36 months of age.
• It is transmitted primarily by direct contact with draining mucosal lesions or from
asymptomatic shedding.
• The incubation period of oral HSV illness is 7 days (range 2 to 25 days).
• Primary HSV infection is more severe than recurrent illness.
• Clinical features of primary HSV gingivostomatitis include:
 high fever,
 poor intake of liquid and solid food,
 dehydration,
 malaise,
 stinging mouth pain,
 drooling,
 fetid breath,
 oropharyngeal vesicular lesions,
 and lymphadenopathy.
• Grouped lesions on an erythematous base are present
around the stomal opening and on the tongue, gums, lips,
and oral mucosa and on the soft and hard palate.
• The lesions usually become crusted and heal within 5 to
10 days, but occasionally they may last 3 weeks.
• Primary infection usually is accompanied by fever and
tender lymphadenopathy, which are often absent with
recurrent disease.
• The lesions persist for 12 days (range 9 to 15 days) and
heal without scarring.
• Limited involvement to only a portion of the vermilion is
more characteristic of recurrent illness than primary HSV
infection; this presentation is often called herpes labialis.
Herpangina
 is an enteroviral infection with major symptoms of sudden onset of
 high fever,
 vomiting,
 headache,
 malaise, myalgia,
 backache,
 conjunctivitis,
 poor intake,
 drooling,
 sore throat, and dysphagia.
 The oral lesions of herpangina may be nonspecific, but classically there are
one or more small, tender, papular, or pinpoint vesicular lesions on an
erythematous base scattered over the soft palate, uvula, fauces, and
tongue.
 These vesicles enlarge from 1 to 2 mm to 3 to 4 mm over 3 to 4 days,
rupture, and produce small, punched-out ulcers that persist for several days.
 LABORATORY EVALUATION

• The principal challenge is to distinguish

pharyngitis caused by group A streptococci
from pharyngitis caused by nonstreptococcal
(usually viral) organisms.
• A rapid streptococcal antigen test or a throat
culture or both are often performed to improve
diagnostic precision and to help identify
children who are most likely to benefit from
antibiotic therapy of streptococcal disease.
• The predictive values of WBC count, ESR, and CRP are not
sufficient to distinguish streptococcal from nonstreptococcal
pharyngitis, and these tests are not routinely recommended.
• The complete blood count in patients with infectious
mononucleosis may show a predominance of atypical
lymphocytes.
• Many rapid diagnostic techniques for streptococcal
pharyngitis are available, with excellent specificity of 95% to
99%.
• The sensitivity of these rapid tests varies, however, and a
negative rapid test ideally should be confirmed with a
negative culture, especially when the clinical suspicion of
streptococcal illness is great.
• Throat culture is the diagnostic "gold standard"
for establishing the presence of streptococcal
pharyngitis.
• False-positive cultures can occur if other
organisms are incorrectly identified as group A
streptococcus.
• A proportion of positive cultures reflects
streptococcal carriage, but not the etiology of
the acute pharyngitis.
 DIFFERENTIAL DIAGNOSIS
• The differential diagnosis of infectious pharyngitis includes
 other local infections of the oral cavity,
 retropharyngeal abscesses (S. aureus, streptococci, anaerobes),
 diphtheria (if unimmunized),
 peritonsillar abscesses (with quinsy sore throat or unilateral tonsil
swelling caused by streptococci, anaerobes, or, rarely, S. aureus),
 and epiglottitis.
 In addition, neutropenic mucositis (leukemia, aplastic anemia), thrush
(candidiasis secondary to T cell immune deficiency), auto-immune
ulceration (systemic lupus erythematosus, Behçet disease), and
Kawasaki disease may cause pharyngitis.
 Pharyngitis is often a prominent feature of EBV-associated
mononucleosis.
• Vincent infection or trench mouth is a
fulminant form of acute necrotizing ulcerative
gingivitis with synergistic infection with
certain spirochetal organisms, notably
Treponema vincentii, with anaerobic
Selenomonas and Fusobacterium.
• Vincent angina refers to a virulent form of
anaerobic pharyngitis wherein gray
pseudomembranes are found on the tonsils,
accounting for the synonym false diphtheria.
• Noma, also known as cancrum oris or gangrenous
stomatitis, may be related in pathophysiology to Vincent
infection, but typically begins as a focal gingival lesion and
rapidly progresses to gangrene and consequent destruction
of bone, teeth, and soft tissues.
• Mortality rates of 70% to 90% occur in the absence of
prompt surgical intervention.
• Noma has been associated with infection by
 Borrelia vincentii
 and Fusobacterium nucleatum.
• Noma seems to be related to
o severe malnutrition
o or to immunodeficiency states.
• Ludwig angina is a mixed anaerobic bacterial cellulitis of
the submandibular and sublingual regions.
• Although often applied to any infection of the sublingual
or submandibular region, the term Ludwig angina
originally was reserved for a rapidly spreading bilateral
cellulitis of the sublingual and submandibular spaces.
• It is often odontogenic in origin, typically spreading from
a periapical abscess of the second or third mandibular
molar. It also has been associated with tongue piercing.
 A propensity for rapid spread, glottic and lingual swelling,
and consequent airway obstruction makes prompt
intervention imperative.
• A syndrome of periodic fever, aphthous stomatitis, pharyngitis, and
cervical adenitis (PFAPA) is a rare cause of recurrent fever in children.
This syndrome is characterized by
 recurring nonspecific pharyngitis
 accompanied by fever and aphthae, which are painful solitary vesicular
lesions in the mouth.
The fevers begin at a young age (usually <5 years old).
• Episodes last approximately 5 days; duration is shorter with treatment
with oral prednisone.
• There is a mean of 28 days between episodes.
• Episodes are unresponsive to non-steroidal anti-inflammatory drugs or
antibiotics.
• The syndrome resolves in some children, whereas symptoms persist in
other children.
• Long-term sequelae do not develop.
 TREATMENT

• Even if untreated, most episodes of streptococcal pharyngitis

resolve uneventfully over a few days.
• If instituted early in the course of illness, however, antimicrobial
therapy accelerates clinical recovery by 12 to 24 hours.
 The major benefit of antimicrobial therapy is the prevention of
acute rheumatic fever.
• Because the latent (incubation) period of acute rheumatic fever is
relatively long (1 to 3 weeks), treatment instituted within 9 days of
illness is virtually 100% successful in preventing rheumatic fever.
Treatment begun more than 9 days after the onset of illness is less
than 100% successful, but may have some preventive value.
• Antibiotic therapy should be started immediately in
children with:
 a positive rapid test for group A streptococcus,
 scarlet fever,
 symptomatic pharyngitis whose siblings are ill with
documented streptococcal pharyngitis,
 symptomatic pharyngitis and a past history of rheumatic
fever or a recent history of rheumatic fever in a family
member,
 or symptomatic pharyngitis who are living in an area
experiencing an epidemic of acute rheumatic fever or
poststreptococcal glomerulonephritis.
• A variety of antimicrobial agents can be used to treat
streptococcal pharyngitis.
• Penicillin has a narrow spectrum, is inexpensive, and has
relatively few adverse effects.
• It usually is given orally three or four times daily for a full
10 days.
• The taste of oral amoxicillin is preferred over oral penicillin
by many children.
• A single IM dose of benzathine penicillin (or a benzathine-
procaine combination) is painful, but it ensures adherence
and provides adequate blood levels for more than 10 days.
• For patients allergic to penicillins, erythromycin is the drug
of choice.
• Some drugs (oral first-generation cephalosporins) seem to
be as good as, or better than, penicillin in eradicating the
streptococci. One proposed explanation is that
staphylococci or anaerobes in the pharynx produce β-
lactamase, which inactivates penicillin and reduces its
efficacy.
• Another possible explanation is that these other drugs are
more effective than penicillin in eradicating streptococcal
carriage. Some drugs also may offer convenience, such as
once-daily administration or shorter length of therapy,
which may translate into improved compliance.
• These drugs are more expensive than penicillin and
usually have more adverse effects.
• Children with recurrent episodes of pharyngitis with
throat cultures positive for group A streptococcus pose
a particular problem. An alternative antibiotic may be
chosen to treat pharyngeal flora producing β-
lactamase, which may be responsible for the
recurrences.
• Either amoxicillin-clavulanate or clindamycin is an
effective regimen for eliminating streptococcal
carriage.
• Specific antiviral therapy is unavailable for most cases
of viral pharyngitis.
• Patients with primary herpetic gingivostomatitis
benefit from early treatment with oral acyclovir.
 COMPLICATIONS AND PROGNOSIS
• Pharyngitis caused by streptococci or respiratory viruses
usually resolves completely.
• The complications of group A streptococcal pharyngitis
include local suppurative complications, such as
parapharyngeal abscess and other infections of the deep
fascial spaces of the neck, and nonsuppurative
complications, such as acute rheumatic fever and acute
postinfectious glomerulonephritis.
• Viral respiratory tract infections, including infections caused
by influenza A, adeno-viruses, parainfluenza type 3, and
rhinoviruses, may predispose to bacterial middle ear infections.
 PREVENTION
• Antimicrobial prophylaxis with daily oral
penicillin prevents recurrent streptococcal
infections and is recommended only to
prevent recurrences of rheumatic fever.