Tonsillitis and Peritonsillar Abscess

Back

Background

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).


View Image

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.

Pathophysiology and Etiology

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:

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 beta-hemolytic 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 tonsils removedfrom 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. Predominant organisms are the anaerobes Prevotella, Porphyromonas, Fusobacterium, and Peptostreptococcus species. Major aerobic organisms are GABHS, S aureus, and H influenzae.

Epidemiology

Tonsillitis most often occurs in children; however, the condition rarely occurs in children younger than 2 years. Tonsillitis caused by Streptococcus species typically occurs in children aged 5-15 years, while viral tonsillitis is more common in younger children. Peritonsillar abscess (PTA) usually occurs in teens or young adults but may present earlier.

Pharyngitis accompanies many upper respiratory tract infections. Between 2.5% and 10.9% of children may be defined as carriers. In one study, the mean prevalence of carrier status of schoolchildren for group A Streptococcus, a cause of tonsillitis, was 15.9%.[5, 6]

According to Herzon et al, children account for approximately one third of peritonsillar abscess episodes in the United States.[7] Recurrent tonsillitis was reported in 11.7% of Norwegian children in one study and estimated in another study to affect 12.1% of Turkish children.[8]

Prognosis

Because of improvements in medical and surgical treatments, complications associated with tonsillitis, including death, are rare.[9] Historically, scarlet fever was a major killer at the beginning of the 20th century, and rheumatic fever was a major cause of cardiac disease and mortality. Although the incidence of rheumatic fever has declined significantly, cases that occurred in the 1980s and early 1990s support concern over a resurgence of this condition.

History

The patient's history determines the type of tonsillitis (ie, acute, recurrent, chronic) that is present.

Individuals with acute tonsillitis present with fever, sore throat, foul breath, dysphagia (difficulty swallowing), odynophagia (painful swallowing), and tender cervical lymph nodes. Airway obstruction may manifest as mouth breathing, snoring, sleep-disordered breathing, nocturnal breathing pauses, or sleep apnea. Lethargy and malaise are common. Symptoms usually resolve in 3-4 days but may last up to 2 weeks despite adequate therapy.

Recurrent streptococcal tonsillitis is diagnosed when an individual has 7 culture-proven episodes in 1 year, 5 infections in 2 consecutive years, or 3 infections each year for 3 years consecutively. Individuals with chronic tonsillitis may present with chronic sore throat, halitosis, tonsillitis, and persistent tender cervical nodes. Children are most susceptible to infection by those in the carrier state.

Individuals with peritonsillar abscess (PTA) present with severe throat pain, fever, drooling, foul breath, trismus (difficulty opening the mouth), and altered voice quality (the hot-potato voice).

Physical Examination

Physical examination should begin by determining the degree of distress regarding airway and swallowing function. Examination of the pharynx may be facilitated by opening the mouth without tongue protrusion, followed by gentle central depression of the tongue. Full assessment of oral mucosa, dentition, and salivary ducts may then be performed by gently "walking" a tongue depressor about the lateral oral cavity. Flexible fiberoptic nasopharyngoscopy may be useful in selected cases, particularly with severe trismus. (The images below depict the oral examination.)


View Image

Examination of the tonsils and pharynx.


View Image

Oral mucosal examination.

Acute tonsillitis

Physical examination in acute tonsillitis reveals fever and enlarged inflamed tonsils that may have exudates (see the image below).


View Image

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

Group A beta-hemolytic Streptococcus pyogenes and Epstein-Barr virus (EBV) can cause tonsillitis that may be associated with the presence of palatal petechiae. Group A beta-hemolytic Streptococcus (GABHS) pharyngitis usually occurs in children aged 5-15 years.

Open-mouth breathing and voice change (ie, a thicker or deeper voice) result from obstructive tonsillar enlargement. The voice change with acute tonsillitis is usually not as severe as that associated with peritonsillar abscess (PTA). In PTA, the pharyngeal edema and trismus cause a hot-potato voice.

Tender cervical lymph nodes and neck stiffness are observed in acute tonsillitis. Examine skin and mucosa for signs of dehydration. Consider infectious mononucleosis due to 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. A gray membrane may cover tonsils that are inflamed from an EBV infection (see the image below). This membrane can be removed without bleeding. Palatal mucosal erosions and mucosal petechiae of the hard palate may also be observed.


View Image

Tonsillitis caused by Epstein-Barr infection (infectious mononucleosis). The enlarged inflamed tonsils are covered with gray-white patches.

HSV pharyngitis

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.

Peritonsillar abscess

Physical examination of a peritonsillar abscess (PTA) almost always reveals unilateral bulging above and lateral to one of the tonsils. Trismus is always present in varying severity. The abscess rarely is located adjacent to the inferior pole of the tonsil. Inferior pole PTA is a difficult diagnosis to make, and radiologic imaging with a contrast-enhanced CT scan is helpful. Tender cervical adenopathy and torticollis (neck turned in the cock-robin position) may be present. Ipsilateral otalgia may be observed.

Complications

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 is Fusobacterium 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.

Approach Considerations

Tonsillitis and peritonsillar abscess (PTA) are clinical diagnoses. Testing is indicated when group A beta-hemolytic 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).

Lab Studies

Throat cultures are the criterion standard for detecting group A beta-hemolytic Streptococcus pyogenes (GABHS). GABHS is the principal organism for which antibiotic therapy (sensitivity 90-95%) is definitely indicated. Growing concerns over bacterial resistance make monitoring acute tonsillitis with throat swabs for culture and sensitivity an important endeavor. Relying only on clinical criteria, such as the presence of exudate, erythema, fever, and lymphadenopathy, is not an accurate method for distinguishing GABHS from viral tonsillitis. A Monospot serum test, CBC count, and serum electrolyte level test may be indicated.

A rapid antigen detection test (RADT), also known as the rapid streptococcal test, detects the presence of GABHS cell wall carbohydrate from swabbed material and is considered less sensitive than throat cultures; however, the test has a specificity of 95% or more and produces a result in significantly less time than that required for throat cultures. A negative RADT requires that a throat culture be obtained before excluding GABHS infection.

A culture or RADT is not indicated in most cases following antibiotic therapy for acute GABHS pharyngitis. Routine testing of asymptomatic household contacts is similarly not usually warranted.

Serum may be examined for antistreptococcal antibodies, including antistreptolysin-O antibodies and antideoxyribonuclease (anti-DNAse) B antibodies. Titers are useful for documenting prior infection in persons diagnosed with acute rheumatic fever, glomerulonephritis, or other complications of GABHS pharyngitis.

Laboratory evaluation in chronic tonsillitis relies upon documentation of results of pharyngeal swabs or cultures taken during prior episodes of tonsillitis. The usefulness and cost of throat swabs for pharyngitis are debated.

Imaging Studies

Routine radiologic imaging is not useful in cases of acute tonsillitis. 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 peritonsillar abscess (PTA), CT scanning with contrast is indicated in general[10] for unusual presentations (eg, an inferior pole abscess) and for patients at high risk for drainage procedures (eg, patients with coagulopathy or anesthetic risk).

CT scanning may be used to guide needle aspiration for draining PTAs after an unsuccessful surgical attempt and for draining abscesses that are located in unusual locations and are anticipated to be difficult to reach with standard surgical approaches.

Approach Considerations

Treatment of acute tonsillitis is largely supportive and focuses on maintaining adequate hydration and caloric intake and controlling pain and fever. Inability to maintain adequate oral caloric and fluid intake may require IV hydration, antibiotics, and pain control. Home intravenous therapy under the supervision of qualified home health providers or the independent oral intake ability of patients ensures hydration. Intravenous corticosteroids may be administered to reduce pharyngeal edema.

Airway obstruction may require management by placing a nasal airway device, using intravenous corticosteroids, and administering humidified oxygen. Observe the patient in a monitored setting until the airway obstruction is clearly resolving.

Tonsillectomy is indicated for individuals who have experienced more than 6 episodes of streptococcal pharyngitis (confirmed by positive culture) in 1 year, 5 episodes in 2 consecutive years, or 3 or more infections of tonsils and/or adenoids per year for 3 years in a row despite adequate medical therapy, or chronic or recurrent tonsillitis associated with the streptococcal carrier state that has not responded to beta-lactamase–resistant antibiotics.

Tonsillitis and its complications are frequently encountered. Antibiotics cure most patients with bacterial tonsillitis, and surgery usually cures patients with infections and complications that are refractory to medical management. Better understanding of the immunology of tonsillitis, actively tracking patterns of bacterial and viral pathogenicity and resistance, and exploring novel technologies for tonsillectomy allow physicians to continue to build on their long experience with these conditions.

Consider transfer of patient care when tonsillitis or its complications cannot be managed safely and expediently. Ensure airway protection for transfer. Ensure that appropriately trained personnel accompany the patient during transfer. Children younger than 3 years may require transfer because of the special care needed during tonsillitis or its complications. Patients with syndromic diagnoses (eg, trisomy 21) and patients with hematologic problems may benefit from transfer to facilities that have the availability of subspecialist care.

Discharge of the patient from the hospital occurs after the patient and caregivers can demonstrate compliance with oral pain medication and antibiotics. To confirm clinical improvement, follow-up care by telephone contact or physical examination may be useful in 2-4 weeks after the acute episode. Follow-up throat swabs and cultures are usually not necessary, unless family or personal history of rheumatic fever exists, significant recurrent tonsillitis is evident, or family members continue to reinfect each other.

Consultations with infectious-disease, hematologic, and pediatric subspecialists are valuable in selected cases.

Corticosteroids

Corticosteroids may shorten the duration of fever and pharyngitis in cases of infectious mononucleosis (MN). In severe cases of MN, corticosteroids or gamma globulin may be helpful. Symptoms of MN may last for several months. Corticosteroids are also indicated for patients with airway obstruction, hemolytic anemia, and cardiac and neurologic disease. Inform patients of complications from steroid use.

Antibiotics

Antibiotics are reserved for secondary bacterial pharyngitis. Because of the risk of a generalized papular rash, avoid ampicillin and related compounds when infectious mononucleosis (MN) is suspected. Similar reactions from oral penicillin–based antibiotics (eg, cephalexin) have been reported. Therefore, initiate therapy with another antistreptococcal antibiotic, such as erythromycin.

Administer antibiotics if conditions support a bacterial etiology, such as the presence of tonsillar exudates, presence of a fever, leukocytosis, contacts who are ill, or contact with a person who has a documented group A beta-hemolytic Streptococcus pyogenes (GABHS) infection. In many cases, bacterial and viral pharyngitis are clinically indistinguishable. Waiting 1-2 days for throat culture results has not been shown to diminish the usefulness of antibiotic therapy in preventing rheumatic fever.

GABHS infection

GABHS infection obligates antibiotic coverage. Bisno et al stated, in a practice guideline for the diagnosis and management of GABHS, that the desired outcomes of therapy for GABHS pharyngitis are the prevention of acute rheumatic fever; the prevention of suppurative complications; abatement of clinical symptoms and signs; reduction in transmission of GABHS to close contacts; and minimization of potential adverse effects of inappropriate antimicrobial therapy.[11]

Administering oral penicillin for 10 days is the best treatment of acute GABHS pharyngitis.[12] Intramuscular penicillin (ie, benzathine penicillin G) is required for persons who may not be compliant with a 10-day course of oral therapy. Penicillin is optimal for most patients (barring allergic reactions) because of its proven safety, efficacy, narrow spectrum, and low cost.

Other antibiotics proven effective for GABHS pharyngitis are the penicillin congeners, many cephalosporins, macrolides, and clindamycin. Clindamycin may be of particular value because its tissue penetration is considered equivalent for both oral and IV administration. Clindamycin is effective even for organisms that are not rapidly dividing (Eagle effect), which explains its great efficacy for GABHS infection. Vancomycin and rifampin have also been useful. Reduced-frequency dosing is recommended to improve compliance with medication regimens. A consensus on the efficacy of such dosing has not yet been formulated.

Most cases of acute pharyngitis are self-limited, with clinical improvement observed in 3-4 days. Clinical practice guidelines state that avoiding antibiotic therapy for this time period is safe and that a delay of up to 9 days from symptom onset to antimicrobial treatment should still prevent the major complication of GABHS (ie, acute rheumatic fever).

Recurrent tonsillitis may be managed with the same antibiotics as acute GABHS pharyngitis. If the infection recurs shortly after a course of an oral penicillin agent, then consider IM benzathine penicillin G. Clindamycin and amoxicillin/clavulanate have been shown to be effective in eradicating GABHS from the pharynx in persons experiencing repeated bouts of tonsillitis. A 3- to 6-week course of an antibiotic against beta-lactamase–producing organisms (eg, amoxicillin/clavulanate) may allow tonsillectomy to be avoided.

Carrier state should be treated when the family has a history of rheumatic fever, a history of glomerulonephritis in the carrier, a "ping pong" spread of infection between household contacts of the carrier, familial anxiety regarding the implications of GABHS carriage, infectious outbreak within a closed community such as a school, an outbreak of acute rheumatic fever, or when tonsillectomy may be under consideration to treat the chronic carriage of GABHS.

Peritonsillar abscess

Peritonsillar cellulitis may respond to oral antibiotics. Antibiotics, either orally or intravenously, are required to treat peritonsillar abscess (PTA) medically, although most PTAs are refractory to antibiotic therapy alone. Penicillin, its congeners (eg, amoxicillin/clavulanic acid, cephalosporins), and clindamycin are appropriate antibiotics. In rare cases of spontaneous PTA rupture, mouthwashes are still recommended for hygienic reasons. A 10-day course of an oral antibiotic is prescribed.

Beta-lactamase resistance

Beta-lactamase resistance of streptococcal species may now be observed in up to a third of community-based streptococcal infections. This resistance is probably due to the presence of copathogens that are beta-lactamase–producing organisms, such as H influenzae and Moraxella catarrhalis. These organisms are able to degrade the beta-lactam ring of penicillin and make an otherwise sensitive GABHS act resistant to beta-lactam antibiotics. In one study, erythromycin did not inhibit nearly half of S pyogenes isolates. The limited precision of many throat swabs may reduce the usefulness of these samples.

Tonsillectomy

Tonsillectomy is indicated for individuals who have experienced more than 6 episodes of streptococcal pharyngitis (confirmed by positive culture) in 1 year, 5 episodes in 2 consecutive years or 3 or more infections for 3 years in a row, or chronic or recurrent tonsillitis associated with the streptococcal carrier state that has not responded to beta-lactamase–resistant antibiotics. Tonsillectomy may be considered for children when multiple antibiotic allergies or intolerances are seen, as well as for children with periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA), or a history of peritonsillar abscess.[13]

Time missed from school or work and severity of illness (eg, whether hospitalization was required) are important considerations in recommending tonsillectomy.

Because adenoid tissue has similar bacteriology to the pharyngeal tonsils and because minimal additional morbidity occurs with adenoidectomy if tonsillectomy is already being performed, most surgeons perform an adenoidectomy if adenoids are present and inflamed at the time of tonsillectomy. However, this point remains controversial.

Recurrent tonsillitis after tonsillectomy is extremely rare. Tonsillectomy reduces the bacterial load of group A beta-hemolytic Streptococcus pyogenes (GABHS) and may also allow an increase in alpha-Streptococcus, which can be protective against GABHS infection. Recurrent tonsillitis is usually due to regrowth of tonsillar tissue, which is treated by excision.

Tonsillectomy with or without adenoidectomy is the treatment of chronic tonsillitis. In cases of chronic tonsillitis, specific technical considerations for tonsillectomy include awareness of a higher intraoperative and perioperative bleeding risk and awareness that dissection may be more difficult because of fibrosis and scarring of the tonsillar capsule. Such considerations may affect instrument selection and discharge decisions.

Surgery is rarely required for acute lingual tonsillitis, but surgery is indicated for frequent and disabling episodes of this uncommon malady. Tonsillar hypertrophy that persists after resolution of mononucleosis and causes obstructive airway symptoms may necessitate tonsillectomy.

Peritonsillar abscess

Treatment of peritonsillar abscess (PTA) includes aspiration and incision and drainage (I&D). The term quinsy tonsillectomy refers to tonsillectomy performed to treat PTA. Bilateral tonsillectomy is usually performed in these cases, and the abscessed tonsil is usually easier to remove during surgery than the inflamed contralateral tonsil. The abscessed tonsil is easier to remove because the abscess partially dissects the tonsil from the pharyngeal musculature.

When PTA is suspected, aspiration with a needle may be attempted to confirm the diagnosis and to remove some of the purulence. The area of the PTA is first anesthetized by infiltration with local anesthetic or by spray or sponge application of topical anesthesia (eg, Americaine, benzocaine). Sedation may be helpful but should be administered only in a facility that is appropriately staffed and equipped.

Tonsillectomy is indicated for PTA associated with chronic or recurrent tonsillitis or for exposure of the abscess in unusual cases. Newer techniques and technologies offer improved recovery and reduced complications from surgery.[14] Acute tonsillectomy is generally regarded as a safe and effective treatment of PTA. Some physicians advocate immediate tonsillectomy for younger patients with PTA. Removing "hot" tonsils (ie, those that are acutely infected) carries the expectation of higher intraoperative blood loss and a higher risk of immediate and delayed post-tonsillectomy hemorrhage.

During surgery, if the abscess cannot be located in the usual superior lateral region of the tonsillar fossa, then careful exploration with needle aspiration may locate the collection, allowing for wide exposure and drainage. Tonsillectomy may be required for exposure in such cases. A CT scan with contrast may be indicated.

Fleshy or pale, granular tonsillar tissue may indicate a neoplasm. Immunohistopathologic examination is indicated in such cases.

Aspiration

An 18-gauge needle on a 1 mL tuberculin syringe is placed into the pointing area, taking care not to penetrate the pharyngeal mucosa more than 1 inch in order to prevent injury to the vessels and nerves of the parapharyngeal space. Bending a sheathed needle at 2 points may prevent deeper injury during aspiration.[15] If attempt at aspiration from 3 different peritonsillar sites does not locate the abscess, the patient should be treated with oral or IV antibiotics. If symptoms persist after 24-48 hours of therapy, CT scanning with contrast may be performed.

Once purulence is detected, complete aspiration may be attempted. Sufficient material should be available for Gram stain and cultures with antibiotic sensitivities. Not all patients need microbiologic evaluation. For those who are immunosuppressed or who have developed a PTA after several days of appropriate antibiotic therapy, aspirated material should be sent for Gram stain, culture, and sensitivity tests.

Incision and drainage

After needle aspiration, incision and drainage may be performed using a knife. The handle of a knife with an attached No. 15 blade is taped 1 inch from the tip to prevent deep penetration through the mucosa. A gentle curvilinear incision, not more than half an inch deep, is fashioned along the perimeter of the tonsillar capsule and through the point from which pus was evacuated. A widely tipped blunt clamp (eg, Kelly clamp) is used to widely open the loculated pockets of purulence. A sponge-covered finger to break loculations is ideal. Rinsing with half-strength hydrogen peroxide solution aids hemostasis. When the patient is dehydrated and uncomfortable, this well-intentioned procedure is not greeted with enthusiasm from the patient.

Sedation, hydration, analgesia, and anesthesia (at the least, topical or local) are important. There may be a role for intravenous dexamethasone in reducing pain after drainage.[16] Some adults and most children require deeper levels of sedation or general anesthesia for safe and adequate aspiration or drainage. An institution with a carefully designed policy for incision and drainage of PTA with conscious sedation, including appropriate indications, staff, and criteria, may offer sedation to children.

Exposure of the posterior oropharynx for aspiration and incision and drainage is achieved by using the nondominant hand to grasp the tongue with a sponge while the patient opens his or her mouth. In patients with severe trismus, a tongue blade may be used to depress the midportion of the tongue. Magnifying and illuminating loupes, such as the LumiView, are the best sources of light. A headlight or mirror is also effective. Arranging the instruments in order of use on a tray adjacent to the physician's dominant hand facilitates rapid accomplishment of this procedure. In experienced hands, this procedure should take fewer than 3 minutes from aspiration to rinsing with peroxide.

After the procedure, the patient is observed in accordance with sedation and anesthetic protocols. Hospitalization for adults and for older children is rarely required. The patient is discharged with a prescription for an oral antibiotic (10-day course of therapy), a prescription for an oral narcotic for pain control (taking care to avoid antiplatelet agents), and instructions to maintain hydration and control fever. Antibiotic therapy may be altered after cultures return. A follow-up office visit or telephone call is made in 2-4 weeks after the procedure to confirm symptomatic resolution.

Diet and Activity

Hydration is important, and the oral route is usually adequate. Intravenous fluids may be required for severe dehydration. Hyperalimentation is rarely necessary. Adequate rest for adults and children with tonsillitis accelerates recovery. In order to reduce risk of splenic rupture in persons diagnosed with systemic mononucleosis, patients must be cautioned against activities that may cause abdominal injury.

Prevention

Avoidance of contact with individuals who are ill or patients who are immunocompromised is useful.

The use of the antipneumococcal vaccine may help to prevent acute tonsillitis; however, to date, experience is insufficient to determine whether prevention is likely to occur.

Medication Summary

Medications that are used to manage tonsillitis include antibiotics, anti-inflammatory agents (eg, corticosteroids), antipyretics and analgesics (eg, acetaminophen, ibuprofen), and immunologic agents (eg, gamma globulin).

Dexamethasone (Baycadron)

Clinical Context:  Dexamethasone is a short-acting, rapid-onset glucocorticoid.

Prednisone

Clinical Context:  Prednisone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisolone (Pediapred, Millipred, Orapred)

Clinical Context:  Prednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli. Corticosteroids reduce inflammation, which may impair swallowing and breathing.

Penicillin G benzathine (Bicillin L-A)

Clinical Context:  Penicillin interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity.

Clarithromycin (Biaxin)

Clinical Context:  Clarithromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. It is a semisynthetic macrolide with twice-daily dosing.

Clindamycin (Cleocin)

Clinical Context:  Clindamycin is an oral or parenteral antibiotic that is used for the treatment of anaerobic or susceptible streptococcal, pneumococcal, or staphylococcal species. It is considered to have good absorption into the bloodstream in both oral and parenteral forms.

Vancomycin

Clinical Context:  Vancomycin is indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. To avoid toxicity, the current recommendation is to assay vancomycin trough levels after the third dose, drawn 30 minutes prior to the next dosing. Use creatinine clearance (CrCl) to adjust the dose in patients diagnosed with renal impairment. It is used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.

Rifampin (Rifadin)

Clinical Context:  Rifampin is an inhibitor of bacterial DNA-dependent RNA polymerase activity.

Amoxicillin (Moxatag)

Clinical Context:  Amoxicillin is an oral antibiotic with specific activity against penicillin-resistant organisms; it is often combined with the beta-lactamase inhibitor clavulanic acid.

Amoxicillin and clavulanate (Augmentin, Amoclan, Augmentin XR)

Clinical Context:  Amoxicillin is a third-generation aminopenicillin. Combined with the beta-lactam clavulanic acid, it is less susceptible to degradation by beta-lactamases produced by microorganisms.

Metronidazole (Flagyl)

Clinical Context:  Metronidazole is effective in patients with tonsillitis and mononucleosis, for shortening fever duration and reducing tonsillar size, and in management of acute episodes of nonstreptococcal tonsillitis.

Ampicillin and sulbactam (Unasyn)

Clinical Context:  This is a drug combination of a beta-lactamase inhibitor with ampicillin. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. It is an alternative to amoxicillin/clavulanate if the patient is unable to take medication orally.

Class Summary

Antibiotic therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Immune globulin intravenous (Gammagard, Gamunex-C, Octagam)

Clinical Context:  Intravenous immune globulin is pooled human immune globulin. Because of a shortage of supply, it is reserved for use for severe infections. It should be used in accordance with institutional policies. Its use in the past was more common for various indications.

Class Summary

These agents are used to improve clinical aspects of the disease. It stimulates immune cells, reducing the severity of infection.

Aspirin (Bayer Aspirin, Ecotrin, Aspercin, Ascriptin, Bufferin)

Clinical Context:  Aspirin lowers elevated body temperature by dilating peripheral vessels, enhancing the dissipation of excess heat. It also acts on the heat-regulating center of the hypothalamus to reduce fever.

Ibuprofen (Motrin, Advil, NeoProfen, Caldolor, Ultraprin)

Clinical Context:  Ibuprofen is one of the few nonsteroidal anti-inflammatory drugs (NSAIDs) indicated for reduction of fever.

Acetaminophen (Tylenol, APAP 500, Mapap, FeverAll)

Clinical Context:  Acetaminophen reduces fever by acting directly on hypothalamic heat-regulating centers, thereby bringing about increased dissipation of body heat with vasodilation and sweating.

Class Summary

Pain and fever control are essential to quality patient care. Analgesics with antipyretic properties ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.

Author

Udayan K Shah, MD, Associate Professor of Otolaryngology-Head and Neck Surgery and Pediatrics, Jefferson Medical College, Thomas Jefferson University; Director, Fellow and Resident Education in Pediatric Otolaryngology, Attending Surgeon, Division of Otolaryngology, Nemours-AI duPont Hospital for Children

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Disclosure: Medvoy Ownership interest Management position; Cerescan Imaging Honoraria Consulting

Additional Contributors

Ari J Goldsmith, MD Chief of Pediatric Otolaryngology, Long Island College Hospital; Associate Professor, Department of Otolaryngology, Division of Pediatric Otolaryngology, State University of New York Downstate Medical Center

Ari J Goldsmith, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American Medical Association, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

  1. Morens DM. Death of a president. N Engl J Med. Dec 9 1999;341(24):1845-9. [View Abstract]
  2. Kean J. Domestic Medical Lectures. Chicago, Ill: 1879.
  3. Woolford TJ, Hanif J, Washband S, Hari CK, Ganguli LA. The effect of previous antibiotic therapy on the bacteriology of the tonsils in children. Int J Clin Pract. Mar 1999;53(2):96-8. [View Abstract]
  4. Bussi M, Carlevato MT, Panizzut B, Omede P, Cortesina G. Are recurrent and chronic tonsillitis different entities? An immunological study with specific markers of inflammatory stages. Acta Otolaryngol Suppl. 1996;523:112-4. [View Abstract]
  5. Pichichero ME, Casey JR. Defining and dealing with carriers of group A Streptococci. Contemporary Pediatrics. 2003;1:46.
  6. Wald ER. Commentary: Antibiotic treatment of pharyngitis. Pediatrics in Review. 2001;22 (8):255-256.
  7. Herzon FS. Harris P. Mosher Award thesis. Peritonsillar abscess: incidence, current management practices, and a proposal for treatment guidelines. Laryngoscope. Aug 1995;105(8 Pt 3 Suppl 74):1-17. [View Abstract]
  8. Kvestad E, Kvaerner KJ, Roysamb E, Tambs K, Harris JR, Magnus P. Heritability of recurrent tonsillitis. Arch Otolaryngol Head Neck Surg. May 2005;131(5):383-7. [View Abstract]
  9. Schmidt RJ, Herzog A, Cook S, O'Reilly R, Deutsch E, Reilly J. Complications of tonsillectomy. Arch Otolaryngol Head and Neck Surg. 2007;133:925-928.
  10. Shah, Udayan K. Peritonsillar and Retropharyngeal Abscess. In: Shah, Samir S. Pediatric Pracice: Infectious Diseases. China: McGraw-Hill; 2009:Chapter 25, pp. 216-22.
  11. Bisno AL, Gerber MA, Gwaltney JM Jr, Kaplan EL, Schwartz RH. Diagnosis and management of group A streptococcal pharyngitis: a practice guideline. Infectious Diseases Society of America. Clin Infect Dis. Sep 1997;25(3):574-83. [View Abstract]
  12. [Guideline] Chiappini E, Regoli M, Bonsignori F, Sollai S, Parretti A, Galli L, et al. Analysis of different recommendations from international guidelines for the management of acute pharyngitis in adults and children. Clin Ther. Jan 2011;33(1):48-58. [View Abstract]
  13. [Guideline] Baugh RF, Archer SM, Mitchell RB, et al. Clinical practice guideline: tonsillectomy in children. Otolaryngol Head Neck Surg. Jan 2011;144(1 Suppl):S1-30. [View Abstract]
  14. Shah, Udayan K. Tonsillectomy & Adenoidectomy: Techniques and Technologies. Madison WI. 2008: Omnipress, Inc. ISBN 978-0-615-23355-0.; 2008.
  15. Sivaji N, Arshad FA, Karkos PD. A novel method of draining a peritonsillar abscess. Clin Otolaryngol. Apr 2011;36(2):189-90. [View Abstract]
  16. Chau JK, Seikaly HR, Harris JR, Villa-Roel C, Brick C, Rowe BH. Corticosteroids in peritonsillar abscess treatment: A blinded placebo-controlled clinical trial. Laryngoscope. Jan 2014;124(1):97-103. [View Abstract]
  17. Adam D, Scholz H, Helmerking M. Comparison of short-course (5 day) cefuroxime axetil with a standard 10 day oral penicillin V regimen in the treatment of tonsillopharyngitis. J Antimicrob Chemother. Feb 2000;45 Suppl:23-30. [View Abstract]
  18. Agren K, Lindberg K, Samulesson A, Blomberg S, Forsgren J, Rynnel-Dagoo B. What is wrong in chronic adenoiditis/tonsillitis immunological factor. Int J Pediatr Otorhinolaryngol. Oct 5 1999;49 Suppl 1:S137-9. [View Abstract]
  19. Berkovitch M, Vaida A, Zhovtis D, Bar-Yohai A, Earon Y, Boldur I. Group A streptococcal pharyngotonsillitis in children less than 2 years of age--more common than is thought. Clin Pediatr (Phila). Jun 1999;38(6):361-3. [View Abstract]
  20. Bisno AL. Acute pharyngitis. N Engl J Med. Jan 18 2001;344(3):205-11. [View Abstract]
  21. Brodsky L. Tonsillitis, tonsillectomy and adenoidectomy. In: Bailey B, Johnson JT, Kohut RI, Pillsbury HC, Tardy ME Jr, eds. Head and Neck surgery-Otolaryngology. Vol 1. Philadelphia, Pa: Lippincott Williams & Wilkins; 1993:833-47.
  22. Brodsky L, Moore L, Stanievich J. The role of Haemophilus influenzae in the pathogenesis of tonsillar hypertrophy in children. Laryngoscope. Oct 1988;98(10):1055-60. [View Abstract]
  23. Brook I. The role of anaerobic bacteria in tonsillitis. Int J Pediatr Otorhinolaryngol. Jan 2005;69(1):9-19. [View Abstract]
  24. Brook I, Gober AE. Interference by aerobic and anaerobic bacteria in children with recurrent group A beta-hemolytic streptococcal tonsillitis. Arch Otolaryngol Head Neck Surg. May 1999;125(5):552-4. [View Abstract]
  25. Brook I, Yocum P, Foote PA Jr. Changes in the core tonsillar bacteriology of recurrent tonsillitis: 1977-1993. Clin Infect Dis. Jul 1995;21(1):171-6. [View Abstract]
  26. Cannon CR, Chambers A. Peritonsillar abscess (PTA) in children. J Miss State Med Assoc. Mar 1999;40(3):78-80. [View Abstract]
  27. Casselbrant ML. What is wrong in chronic adenoiditis/tonsillitis anatomical considerations. Int J Pediatr Otorhinolaryngol. Oct 5 1999;49 Suppl 1:S133-5. [View Abstract]
  28. Cohen JI. Epstein-Barr virus infection. N Engl J Med. Aug 17 2000;343(7):481-92. [View Abstract]
  29. Curtin JM. The history of tonsil and adenoid surgery. Otolaryngol Clin North Am. May 1987;20(2):415-9. [View Abstract]
  30. Dhawan B, Chaudhry R, Pandey A, Nisar N, Singh M. Anaerobic septicaemia by Fusobacterium necrophorum: Lemierre's syndrome. Indian J Pediatr. May-Jun 1998;65(3):469-72. [View Abstract]
  31. Gerber MA. Streptococcal infections: Group A B-hemolytic streptococci. In: Rudolph AM, Hoffman JIE, Rudolph CD, eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 604-9.
  32. Handler SD, Myer CM III. Atlas of Ear, Nose and Throat Disorders in Children. Hamilton, Ontario: BC Decker; 1998:91.
  33. Krauss B, Green SM. Sedation and analgesia for procedures in children. N Engl J Med. Mar 30 2000;342(13):938-45. [View Abstract]
  34. Kvestad E, Kvaerner KJ, Roysamb E, Tambs K, Harris JR, Magnus P. Heritability of recurrent tonsillitis. Arch Otolaryngol Head Neck Surg. May 2005;131(5):383-7. [View Abstract]
  35. Lan AJ, Colford JM, Colford JM Jr. The impact of dosing frequency on the efficacy of 10-day penicillin or amoxicillin therapy for streptococcal tonsillopharyngitis: A meta-analysis. Pediatrics. Feb 2000;105(2):E19. [View Abstract]
  36. Lascaratos J, Assimakopoulos D. Surgery on the larynx and pharynx in Byzantium (AD 324-1453): early scientific descriptions of these operations. Otolaryngol Head Neck Surg. Apr 2000;122(4):579-83. [View Abstract]
  37. Licameli GR, Grillone GA. Inferior pole peritonsillar abscess. Otolaryngol Head Neck Surg. Jan 1998;118(1):95-9. [View Abstract]
  38. Lilja M, Silvola J, Bye HM, Raisanen S, Stenfors LE. SIgA- and IgG-coated Streptococcus pyogenes on the tonsillar surfaces during acute tonsillitis. Acta Otolaryngol. 1999;119(6):718-23. [View Abstract]
  39. Lomat L, Galburt G, Quastel MR, Polyakov S, Okeanov A, Rozin S. Incidence of childhood disease in Belarus associated with the Chernobyl accident. Environ Health Perspect. Dec 1997;105 Suppl 6:1529-32. [View Abstract]
  40. Lopez-Gonzalez MA, Lucas M, Mata F, Delgado F. Microalbuminuria as renal marker in recurrent acute tonsillitis and tonsillar hypertrophy in children. Int J Pediatr Otorhinolaryngol. Oct 25 1999;50(2):119-24. [View Abstract]
  41. Manecke GR Jr, Marghoob S, Finzel KC, Madoff DC, Quijano IH, Poppers PJ. Catastrophic caudad spread of a peritonsillar abscess: a case report. Anesthesiology. Dec 1999;91(6):1956-8. [View Abstract]
  42. Martin JM, Green M, Barbadora KA, Wald ER. Group A streptococci among school-aged children: clinical characteristics and the carrier state. Pediatrics. Nov 2004;114(5):1212-9. [View Abstract]
  43. Nord CE. The role of anaerobic bacteria in recurrent episodes of sinusitis and tonsillitis. Clin Infect Dis. Jun 1995;20(6):1512-24. [View Abstract]
  44. Puchalski R, Shah UK. Plasma-mediated ablation for the management of obstructive sleep apnea. In: Anderson R, et al, eds. Lasers in Surgery: Advanced Characterization, Therapeutics, and Systems X. Proceedings of SPIE. Vol 3907. 2000:317-20.
  45. Raut VV, Yung MW. Peritonsillar abscess: the rationale for interval tonsillectomy. Ear Nose Throat J. Mar 2000;79(3):206-9. [View Abstract]
  46. Roberson DW, Kirse DJ. Infectious and inflammatory disorders of the neck. In: Wetmore RF, Muntz HR, McGill TJ. Pediatric Otolaryngology: Principles and Practical Pathways. New York, NY: Thieme; 2000:969-991.
  47. Robinson AC, Hanif J, Dumbreck LA, Prichard AJ, Manners BT. Throat swabs in chronic tonsillitis: a time-honoured practice best forgotten. Br J Clin Pract. Apr-May 1997;51(3):138-9. [View Abstract]
  48. Sancho LM, Minamoto H, Fernandez A, Sennes LU, Jatene FB. Descending necrotizing mediastinitis: a retrospective surgical experience. Eur J Cardiothorac Surg. Aug 1999;16(2):200-5. [View Abstract]
  49. Shah UK, Tufano RP, Handler SD. Post-tonsillectomy observation and admission: Annual Meeting of the American Academy of Pediatrics. In: an American Society of Pediatric Otolaryngology (ASPO) member survey. Paper presented at: Washington, DC; 1999.
  50. Skitarelic N, Mladina R, Matulic Z, Kovacic M. Necrotizing fasciitis after peritonsillar abscess in an immunocompetent patient. J Laryngol Otol. Aug 1999;113(8):759-61. [View Abstract]
  51. Smitheringdale AJ. Acquired diseases of the oral cavity and pharynx. In: Wetmore RF, Muntz HR, McGill TJ. Pediatric Otolaryngology: Principles and Practical Pathways. New York, NY: Thieme; 2000:606-18.
  52. Stjernquist-Desatnik A, Holst E. Tonsillar microbial flora: comparison of recurrent tonsillitis and normal tonsils. Acta Otolaryngol. Jan 1999;119(1):102-6. [View Abstract]
  53. Suskind DL, Park J, Piccirillo JF, Lusk RP, Muntz HR. Conscious sedation: a new approach for peritonsillar abscess drainage in the pediatric population. Arch Otolaryngol Head Neck Surg. Nov 1999;125(11):1197-200. [View Abstract]
  54. Suzuki M, Ueyama T, Mogi G. Immediate tonsillectomy for peritonsillar abscess. Auris Nasus Larynx. Jul 1999;26(3):299-304. [View Abstract]
  55. Wolf M, Kronenberg J, Kessler A, Modan M, Leventon G. Peritonsillar abscess in children and its indication for tonsillectomy. Int J Pediatr Otorhinolaryngol. Nov 1988;16(2):113-7. [View Abstract]
  56. Yoda K, Sata T, Kurata T, Aramaki H. Oropharyngotonsillitis associated with nonprimary Epstein-Barr virus infection. Arch Otolaryngol Head Neck Surg. Feb 2000;126(2):185-93. [View Abstract]

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

Examination of the tonsils and pharynx.

Oral mucosal examination.

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

Tonsillitis caused by Epstein-Barr infection (infectious mononucleosis). The enlarged inflamed tonsils are covered with gray-white patches.

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

Tonsillitis caused by Epstein-Barr infection (infectious mononucleosis). The enlarged inflamed tonsils are covered with gray-white patches.

Examination of the tonsils and pharynx.

Oral mucosal examination.