In the first century AD, Celsus described tonsillectomy performed with sharp tools and followed by rinses

with vinegar and other medicinals. Since that time, physicians have been documenting management of
tonsillitis. Tonsillitis gained additional attention as a medical concern in the late 19th century. The
consideration of quinsy in the differential diagnosis of George Washington's death and the discussion of
tonsillitis in Kean's Domestic Medical Lectures, a home medical companion book published in the late
19th century, reflect the rise of tonsillitis as a medical concern. [1, 2]
Understanding the disease process and management of this common malady remain important today.
This article summarizes the current management of tonsillitis and highlights recent advances in the
pathophysiology and immunology of this condition and its variations: acute tonsillitis (see the image
below), recurrent tonsillitis, and chronic tonsillitis and peritonsillar abscess (PTA).

Acute bacterial tonsillitis is shown. The tonsils are enlarged and inflamed with
exudates. The uvula is midline.

Definitions
Tonsillitis is inflammation of the pharyngeal tonsils. The inflammation usually extends to the adenoid and
the lingual tonsils; therefore, the term pharyngitis may also be used. Pharyngotonsillitis and
adenotonsillitis are considered equivalent for the purposes of this article. Lingual tonsillitis refers to
isolated inflammation of the lymphoid tissue at the tongue base.
A "carrier state" is defined by a positive pharyngeal culture of group A beta hemolytic Streptococcus
pyogenes (GABHS), without evidence of an antistreptococcal immunologic response.
Viral or bacterial infections and immunologic factors lead to tonsillitis and its complications. Overcrowded
conditions and malnourishment promote tonsillitis. Most episodes of acute pharyngitis and acute tonsillitis
are caused by viruses such as the following:

Herpes simplex virus

Epstein-Barr virus (EBV)
Cytomegalovirus
Other herpes viruses
Adenovirus
Measles virus
In one study showing that EBV may cause tonsillitis in the absence of systemic mononucleosis, EBV was
found to be responsible for 19% of exudative tonsillitis in children.
Bacteria cause 15-30% of cases of pharyngotonsillitis. Anaerobic bacteria play an important role in
tonsillar disease. Most cases of bacterial tonsillitis are caused by group A beta-hemolytic Streptococcus
pyogenes (GABHS). S pyogenes adheres to adhesin receptors that are located on the tonsillar
epithelium. Immunoglobulin coating of pathogens may be important in the initial induction of bacterial
tonsillitis.
Mycoplasma pneumoniae, Corynebacterium diphtheriae, and Chlamydia pneumoniae rarely cause acute
pharyngitis. Neisseria gonorrhea may cause pharyngitis in sexually active persons. Arcanobacterium
haemolyticum is an important cause of pharyngitis in Scandinavia and the United Kingdom but is not

recognized as such in the United States. A rash similar to that of scarlet fever accompanies A
haemolyticum pharyngitis.

Recurrent tonsillitis
A polymicrobial flora consisting of both aerobic and anaerobic bacteria has been observed in core tonsillar
cultures in cases of recurrent pharyngitis, and children with recurrent GABHS tonsillitis have different
bacterial populations than children who have not had as many infections. Other competing bacteria are
reduced, offering less interference to GABHS infection. Streptococcus pneumoniae, Staphylococcus
aureus, and Haemophilus influenzae are the most common bacteria isolated in recurrent tonsillitis,
and Bacteroides fragilis is the most common anaerobic bacterium isolated in recurrent tonsillitis.
The microbiologies of recurrent tonsillitis in children and adults are different; adults show more bacterial
isolates, with a higher recovery rate of Prevotella species,Porphyromonas species, and B
fragilis organisms , whereas children show more GABHS. Also, adults more often have bacteria that
produce beta-lactamase.

Chronic tonsillitis
A polymicrobial bacterial population is observed in most cases of chronic tonsillitis, with alpha- and betahemolytic streptococcal species, S aureus, H influenzae, and Bacteroides species having been identified.
A study that was based on bacteriology of the tonsillar surface and core in 30 children undergoing
tonsillectomy suggested that antibiotics prescribed 6 months before surgery did not alter the tonsillar
bacteriology at the time of tonsillectomy.[3] A relationship between tonsillar size and chronic bacterial
tonsillitis is believed to exist. This relationship is based on both the aerobic bacterial load and the absolute
number of B and T lymphocytes. H influenzae is the bacterium most often isolated in hypertrophic tonsils
and adenoids. With regard to penicillin resistance or beta-lactamase production, the microbiology of
tonsils removed from patients with recurrent GABHS pharyngitis has not been shown to be significantly
different from the microbiology of tonsilsremovedfrom patients with tonsillar hypertrophy.
Local immunologic mechanisms are important in chronic tonsillitis. The distribution of dendritic cells and
antigen-presenting cells is altered during disease, with fewer dendritic cells on the surface epithelium and
more in the crypts and extrafollicular areas. Study of immunologic markers may permit differentiation
between recurrent and chronic tonsillitis. Such markers in one study indicated that children more often
experience recurrent tonsillitis, whereas adults requiring tonsillectomy more often experience chronic
tonsillitis.[4]
Radiation exposure may relate to the development of chronic tonsillitis. A high prevalence of chronic
tonsillitis was noted following the Chernobyl nuclear reactor accident in the former Soviet Union.

Peritonsillar abscess
A polymicrobial flora is isolated from peritonsillar abscesses (PTAs). Predominant organisms are the
anaerobes Prevotella, Porphyromonas, Fusobacterium, andPeptostreptococcus species. Major aerobic
organisms are GABHS, S aureus, and H influenzae.
Uhler et al, in an analysis of data from 460 patients with PTA, found a higher incidence of the condition in
smokers than in nonsmokers.[5]

Diagnostic Considerations
Consider infectious mononucleosis (MN) due to Epstein-Barr virus (EBV) in an adolescent or younger
child with acute tonsillitis, particularly when it is accompanied by tender cervical, axillary, and/or inguinal
nodes; splenomegaly; severe lethargy and malaise; and low-grade fever.

An individual with herpes simplex virus (HSV) pharyngitis presents with red, swollen tonsils that may have
aphthous ulcers on their surfaces. Herpetic gingival stomatitis, herpes labialis, and hypopharyngeal and
epiglottic lesions may be observed.

Differential Diagnoses

Gastroesophageal Reflux Disease

Leukemias
Lymphomas of the Head and Neck
Malignant Nasopharyngeal Tumors
Malignant Tumors of the Tonsil

Approach Considerations
Tonsillitis and peritonsillar abscess (PTA) are clinical diagnoses. Testing is indicated when group A betahemolytic Streptococcus pyogenes (GABHS) infection is suspected. Throat cultures are the criterion
standard for detecting GABHS. For patients in whom acute tonsillitis is suspected to have spread to deep
neck structures (ie, beyond the fascial planes of the oropharynx), radiologic imaging using plain films of
the lateral neck or CT scans with contrast is warranted. In cases of PTA, CT scanning with contrast is
indicated.
Test the patient's family members for the presence of streptococcal antibodies to detect carriers of group
A Streptococcus (especially family members who are immunocompromised).
Be vigilant for signs of impending complications from tonsillitis (eg, mental status changes, severe
trismus, high fevers). When necessary, perform further tests or other diagnostic evaluations (eg, CBC
counts, CT scanning) in patients with signs of impending complications from tonsillitis.
Treatment of suspected streptococcal pharyngitis with appropriate antibiotics may lead to complications,
such as acute rheumatic fever and glomerulonephritis.

Acute tonsillitis
Untreated or incompletely treated tonsillitis can lead to potentially life-threatening complications. Acute
oropharyngeal infections can spread distally to the deep neck spaces and then into the mediastinum.
Such complications may require thoracotomy and cervical exposure for drainage. Spread beyond the
pharynx is suspected in persons with symptoms of tonsillitis who also have high or spiking fevers,
lethargy, torticollis, trismus, or shortness of breath. Radiologic imaging using plain films of the lateral neck
or CT scans with contrast is warranted for patients in whom deep neck spread of acute tonsillitis (beyond
the fascial planes of the oropharynx) is suspected.
The most common complication is adjacent spread just beyond the tonsillar capsule. Peritonsillar cellulitis
develops when inflammation spreads beyond the lymphoid tissue of the tonsil to involve the
oropharyngeal mucosa. Peritonsillar abscess (PTA), historically referred to as quinsy, is caused by
purulence trapped between the tonsillar capsule and the lateral pharyngeal wall; the superior constrictor
muscle primarily comprises the lateral pharyngeal wall in this area. Most often, PTA spreads into the
retropharyngeal space or into the parapharyngeal space. Spread may result in necrotizing fasciitis.

Treatment includes IV antibiotics, surgical debridement, and, in cases of associated toxic shock
syndrome, possibly IV immunoglobulins. Distal abscess spread can be life threatening.
Rarely, acute pharyngotonsillitis may lead to thrombophlebitis of the internal jugular vein (Lemierre
syndrome). The usual cause of this condition isFusobacterium necrophorum. A patient who appears toxic
following tonsillitis presents with spiking fevers and unilateral neck fullness and tenderness. CT scanning
with contrast is necessary to help make the diagnosis. A prolonged course of IV antibiotics and treatment
of the source of infection (eg, an abscess) are required. Anticoagulation is controversial. Ligation or
excision of the internal jugular vein is required after multiple septic emboli become evident.

GABHS pharyngitis
Complications specific to group A beta-hemolytic Streptococcus pyogenes(GABHS) pharyngitis are
scarlet fever, rheumatic fever, septic arthritis, and glomerulonephritis.
Scarlet fever
Scarlet fever manifests as a generalized, nonpruritic, macular erythematous rash that is worse on the
extremities and spares the face. The classic strawberry tongue is bright red and tender because of
papillary desquamation. The rash lasts up to 1 week and is accompanied by fever and arthralgias.
Individuals at risk for this rash are those who do not have antitoxin antibodies to the exotoxin produced by
GABHS.
Acute poststreptococcal glomerulonephritis
Acute poststreptococcal glomerulonephritis (AGN) occurs in 10-15% of pharyngitis cases that are caused
by the type-12 serotype. AGN follows GABHS by 1-2 weeks. Urinalysis to detect excreted protein may
allow detection of subclinical renal injury for persons with recurrent tonsillitis.
Rheumatic fever
Rheumatic fever follows acute pharyngitis by 2-4 weeks and was observed in up to 3% of streptococcal
pharyngitides in the mid-20th century. Today, far fewer persons experience this complication, largely
because of appropriate antibiotic therapy. Cardiac valvular vegetations affect the mitral and tricuspid
valves, leading to murmurs, persistent relapsing fevers, and valvular stenosis or incompetence. A throat
swab does not identify the causative organism, because a positive result may reflect colonization rather
than pathogenicity. Elevated or rising titers of antistreptolysin (ASO) antibodies, anti-DNAse beta, or
antihyaluronidase are required to make the diagnosis.
Septic arthritis
Septic arthritis results in a painful hot joint that contains fluid with bacteria. Arthrocentesis is diagnostic
and partially therapeutic. Treatment with IV antibiotics for 6 weeks is required to prevent long-term joint
complications.