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.

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)
Other herpes viruses
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
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

and betahemolytic streptococcal species.Porphyromonas species. with alpha. Other competing bacteria are reduced. Predominant organisms are the anaerobes Prevotella. Study of immunologic markers may permit differentiation between recurrent and chronic tonsillitis. Streptococcus pneumoniae. in an analysis of data from 460 patients with PTA.recognized as such in the United States. adults show more bacterial isolates. S aureus. . splenomegaly. H influenzae. Uhler et al. andPeptostreptococcus species. Porphyromonas. and Bacteroides species having been identified. The distribution of dendritic cells and antigen-presenting cells is altered during disease.[4] Radiation exposure may relate to the development of chronic tonsillitis. found a higher incidence of the condition in smokers than in nonsmokers. Staphylococcus aureus. Such markers in one study indicated that children more often experience recurrent tonsillitis. whereas adults requiring tonsillectomy more often experience chronic tonsillitis. and H influenzae. severe lethargy and malaise. A rash similar to that of scarlet fever accompanies A haemolyticum pharyngitis. whereas children show more GABHS. particularly when it is accompanied by tender cervical. 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. With regard to penicillin resistance or beta-lactamase production. The microbiologies of recurrent tonsillitis in children and adults are different. Chronic tonsillitis A polymicrobial bacterial population is observed in most cases of chronic tonsillitis. and Haemophilus influenzae are the most common bacteria isolated in recurrent tonsillitis. offering less interference to GABHS infection. and Bacteroides fragilis is the most common anaerobic bacterium isolated in recurrent tonsillitis. with a higher recovery rate of Prevotella species. A high prevalence of chronic tonsillitis was noted following the Chernobyl nuclear reactor accident in the former Soviet Union.[3] A relationship between tonsillar size and chronic bacterial tonsillitis is believed to exist. adults more often have bacteria that produce beta-lactamase. and B fragilis organisms . with fewer dendritic cells on the surface epithelium and more in the crypts and extrafollicular areas. 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. axillary. and/or inguinal nodes. Recurrent tonsillitis A polymicrobial flora consisting of both aerobic and anaerobic bacteria has been observed in core tonsillar cultures in cases of recurrent pharyngitis. Fusobacterium. Peritonsillar abscess A polymicrobial flora is isolated from peritonsillar abscesses (PTAs). This relationship is based on both the aerobic bacterial load and the absolute number of B and T lymphocytes. and children with recurrent GABHS tonsillitis have different bacterial populations than children who have not had as many infections. Major aerobic organisms are GABHS. H influenzae is the bacterium most often isolated in hypertrophic tonsils and adenoids. Also. and low-grade fever.[5] Diagnostic Considerations Consider infectious mononucleosis (MN) due to Epstein-Barr virus (EBV) in an adolescent or younger child with acute tonsillitis. S aureus. Local immunologic mechanisms are important in chronic tonsillitis.

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. When necessary. 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 superior constrictor muscle primarily comprises the lateral pharyngeal wall in this area. Spread may result in necrotizing fasciitis. lethargy. herpes labialis. trismus. The most common complication is adjacent spread just beyond the tonsillar capsule. Be vigilant for signs of impending complications from tonsillitis (eg. CT scanning) in patients with signs of impending complications from tonsillitis. Treatment of suspected streptococcal pharyngitis with appropriate antibiotics may lead to complications. CT scanning with contrast is indicated. swollen tonsils that may have aphthous ulcers on their surfaces. For patients in whom acute tonsillitis is suspected to have spread to deep neck structures (ie.An individual with herpes simplex virus (HSV) pharyngitis presents with red. perform further tests or other diagnostic evaluations (eg. Spread beyond the pharynx is suspected in persons with symptoms of tonsillitis who also have high or spiking fevers. Peritonsillar abscess (PTA). Acute oropharyngeal infections can spread distally to the deep neck spaces and then into the mediastinum. In cases of PTA. severe trismus. mental status changes. Such complications may require thoracotomy and cervical exposure for drainage. Acute tonsillitis Untreated or incompletely treated tonsillitis can lead to potentially life-threatening complications. such as acute rheumatic fever and glomerulonephritis. 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). or shortness of breath. Most often. and hypopharyngeal and epiglottic lesions may be observed. torticollis. beyond the fascial planes of the oropharynx). Peritonsillar cellulitis develops when inflammation spreads beyond the lymphoid tissue of the tonsil to involve the oropharyngeal mucosa. . high fevers). radiologic imaging using plain films of the lateral neck or CT scans with contrast is warranted. historically referred to as quinsy. PTA spreads into the retropharyngeal space or into the parapharyngeal space. Throat cultures are the criterion standard for detecting GABHS. is caused by purulence trapped between the tonsillar capsule and the lateral pharyngeal wall. Herpetic gingival stomatitis. Testing is indicated when group A betahemolytic Streptococcus pyogenes (GABHS) infection is suspected. CBC counts.

Septic arthritis Septic arthritis results in a painful hot joint that contains fluid with bacteria. Anticoagulation is controversial. Cardiac valvular vegetations affect the mitral and tricuspid valves. surgical debridement. septic arthritis. possibly IV immunoglobulins. Distal abscess spread can be life threatening. persistent relapsing fevers. largely because of appropriate antibiotic therapy. Elevated or rising titers of antistreptolysin (ASO) antibodies. Today. nonpruritic. Rarely. rheumatic fever. Treatment with IV antibiotics for 6 weeks is required to prevent long-term joint complications. in cases of associated toxic shock syndrome. leading to murmurs. A patient who appears toxic following tonsillitis presents with spiking fevers and unilateral neck fullness and tenderness. far fewer persons experience this complication. and glomerulonephritis. GABHS pharyngitis Complications specific to group A beta-hemolytic Streptococcus pyogenes(GABHS) pharyngitis are scarlet fever. Arthrocentesis is diagnostic and partially therapeutic. and. 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. The usual cause of this condition isFusobacterium necrophorum. acute pharyngotonsillitis may lead to thrombophlebitis of the internal jugular vein (Lemierre syndrome). A throat swab does not identify the causative organism. Acute poststreptococcal glomerulonephritis Acute poststreptococcal glomerulonephritis (AGN) occurs in 10-15% of pharyngitis cases that are caused by the type-12 serotype. an abscess) are required. . AGN follows GABHS by 1-2 weeks. The classic strawberry tongue is bright red and tender because of papillary desquamation. because a positive result may reflect colonization rather than pathogenicity. CT scanning with contrast is necessary to help make the diagnosis. macular erythematous rash that is worse on the extremities and spares the face. anti-DNAse beta. Individuals at risk for this rash are those who do not have antitoxin antibodies to the exotoxin produced by GABHS. Ligation or excision of the internal jugular vein is required after multiple septic emboli become evident. A prolonged course of IV antibiotics and treatment of the source of infection (eg. or antihyaluronidase are required to make the diagnosis. and valvular stenosis or incompetence. Scarlet fever Scarlet fever manifests as a generalized.Treatment includes IV antibiotics. Urinalysis to detect excreted protein may allow detection of subclinical renal injury for persons with recurrent tonsillitis. The rash lasts up to 1 week and is accompanied by fever and arthralgias.