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Tonsillitis

Tonsillitis is an inflammation of the tonsils, which are two oval-shaped masses of lymphoid tissue located at the back of the throat on either side of the tongue.^[1] It most commonly affects children between the ages of 5 and 15, though it can occur at any age, and accounts for approximately 2% of outpatient visits in the United States.^[2] The condition is typically caused by viral or bacterial infections, with viruses responsible for the majority of cases and group A Streptococcus (strep throat) being the most frequent bacterial culprit.^[1] Common symptoms include a sore throat, difficulty swallowing, red and swollen tonsils often coated with white or yellow pus, fever, enlarged tender lymph nodes in the neck, headache, and bad breath; young children may also exhibit fussiness, drooling, or refusal to eat.^[1] Diagnosis usually involves a physical examination of the throat and a rapid strep test or throat culture to identify bacterial infection, with blood tests occasionally used to differentiate viral from bacterial causes.^[3] Treatment depends on the underlying cause: viral tonsillitis generally resolves within 7 to 10 days with supportive care such as rest, hydration, saltwater gargles, over-the-counter pain relievers like acetaminophen or ibuprofen, and throat lozenges for those over age 4.^[3] Bacterial cases, particularly those due to group A strep, require antibiotics such as penicillin for 10 days to prevent complications like rheumatic fever or peritonsillar abscess.^[3] In recurrent or severe cases—defined as seven episodes in one year, five per year for two years, or three per year for three years—a tonsillectomy may be recommended to remove the tonsils and reduce future infections.^[3]^[2] Complications are rare but can include obstructive sleep apnea from enlarged tonsils, spreading infection leading to cellulitis or abscess, or post-streptococcal issues such as kidney inflammation or scarlet fever if untreated.^[1] Prevention focuses on hygiene practices, including frequent handwashing, avoiding close contact with infected individuals, not sharing utensils or food, and keeping children home from school when ill.^[1]

Anatomy and Physiology

Structure of the Tonsils

The tonsils form a key component of Waldeyer's ring, a circular arrangement of lymphoid tissue encircling the pharynx at the junction of the respiratory and digestive tracts. This ring consists of the palatine tonsils, pharyngeal tonsils (adenoids), lingual tonsils, and tubal tonsils. The palatine tonsils, the most prominent and commonly referenced, are paired oval masses situated bilaterally in the oropharynx between the anterior (palatoglossal) and posterior (palatopharyngeal) tonsillar pillars, projecting into the tonsillar fossae.^[4]^[5] These tonsils are composed of dense lymphoid tissue encapsulated laterally by a thin fibrous capsule, while their medial surfaces are exposed to the oropharyngeal lumen. The exposed surface is covered by non-keratinized stratified squamous epithelium, which invaginates deeply to form 10 to 20 branched crypts per tonsil; these crypts increase the surface area for contact with luminal contents and facilitate the trapping of particulate matter, including pathogens. The tonsils receive their blood supply primarily from the tonsillar branches of the maxillary artery and the ascending palatine artery, with venous drainage via the peritonsillar plexus. Innervation is provided by the glossopharyngeal nerve (sensory) and branches of the vagus nerve.^[4]^[5] Microscopically, the tonsillar parenchyma is organized into lymphoid follicles, each featuring a germinal center surrounded by a mantle zone of lymphocytes. The germinal centers contain proliferating B cells undergoing somatic hypermutation and affinity maturation. The crypt epithelium includes specialized microfold (M) cells, which sample antigens from the oropharyngeal lumen and transport them to underlying immune cells for presentation. This structural arrangement positions the tonsils as a frontline interface between external environments and systemic immunity.^[4]^[5] Tonsillar size varies significantly with age, reflecting developmental changes in lymphoid tissue. They begin forming during the second trimester of gestation from the endoderm of the second pharyngeal pouch, with lymphoid tissue derived from mesodermal precursors, becoming prominent postnatally. Hypertrophy peaks between ages 4 and 12 years, significantly narrowing the oropharyngeal airway, before gradual involution begins around puberty, leading to atrophy in adulthood.^[4]^[6]

Function in Immunity

The tonsils serve as a critical component of the mucosa-associated lymphoid tissue (MALT), forming part of Waldeyer's ring that encircles the oropharynx and nasopharynx to provide mucosal immunity at the interface between the respiratory and digestive tracts.^[7] As such, they function as sentinel structures that sample antigens from inhaled or ingested pathogens, primarily through their epithelial crypts and specialized microfold (M) cells, which facilitate the uptake and transport of these antigens to underlying lymphoid tissues for processing by antigen-presenting cells.^[8] This localized antigen sampling initiates adaptive immune responses without allowing widespread dissemination, effectively trapping and neutralizing potential threats at the mucosal surface.^[7] Within the tonsillar architecture, germinal centers host B-cell proliferation and differentiation, leading to the production of secretory IgA antibodies that coat mucosal surfaces and neutralize pathogens locally.^[8] Concurrently, T cells, including CD4+ helper and CD8+ cytotoxic subsets, become activated in these centers to orchestrate humoral and cellular immunity, promoting class-switch recombination in B cells and the generation of memory lymphocytes that prevent systemic infection spread.^[7] These mechanisms ensure a rapid, targeted response that bolsters overall mucosal defense. Tonsillar hypertrophy is particularly prominent in early childhood, peaking between ages 3 and 7 years, as frequent exposure to environmental antigens drives lymphoid hyperplasia and contributes to the maturation of the adaptive immune system during this vulnerable period.^[8]

Pathophysiology

Acute Inflammation

Acute tonsillitis begins with microbial invasion of the tonsillar crypt epithelium, a structure characterized by invaginations that facilitate entry of pathogens into the lymphoid tissue. This invasion triggers an immediate inflammatory response, including local edema due to increased vascular permeability, vasodilation of tonsillar blood vessels, and rapid neutrophil infiltration to combat the infection.^[2]^[9] The inflammatory cascade is amplified by the release of pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) from activated macrophages and epithelial cells. These cytokines promote hyperemia through further vasodilation, stimulate exudate formation by attracting additional immune cells and plasma proteins, and contribute to pain via irritation of local sensory nerves. Neutrophil chemokines like IL-8, induced by IL-1 and TNF-α, enhance neutrophil recruitment and activation, leading to the accumulation of these cells in the tonsillar crypts.^[10]^[9] The condition progresses from superficial epithelial infection to deeper lymphoid hyperplasia within 24-48 hours, as lymphocytes proliferate in response to the antigen. Resolution typically occurs in 7-10 days through programmed neutrophil apoptosis followed by phagocytosis by macrophages, restoring tissue homeostasis without long-term damage.^[2] Unlike pharyngitis, which involves diffuse inflammation of the pharyngeal mucosa, acute tonsillitis features specific involvement of the tonsillar crypts, often resulting in crypt abscesses filled with neutrophils and debris that characterize the localized bacterial response.^[11]

Chronic Changes

Chronic changes in the tonsils often arise from recurrent acute tonsillitis, defined as multiple episodes such as five or more occurrences per year, leading to cumulative tissue damage in the palatine tonsils.^[2] Chronic tonsillitis itself refers to persistent inflammation lasting more than two weeks, while recurrent episodes contribute to long-term structural alterations.^[12] This progression often involves criteria such as 5-7 episodes annually over 1-2 years, resulting in structural alterations that perpetuate the condition.^[13] Recurrent infections promote tonsillar hypertrophy, observed in up to 82% of chronic cases, characterized by enlarged lymphoid follicles and increased tonsillar volume due to persistent antigenic stimulation.^[14] Accompanying this is crypt dilation, where the invaginated surfaces of the tonsils become hyperemic and widened, creating niches for microbial persistence.^[14] Within these dilated crypts, biofilm formation is prevalent, affecting 70.8% of chronic tonsillitis specimens, with bacteria such as Staphylococcus aureus forming robust polysaccharide matrices that shield pathogens from antibiotics and host immunity.^[15] These biofilms, detected in 73% of recurrent tonsillitis cases via electron microscopy, contribute to the chronicity by enabling low-grade, persistent colonization.^[16] Over time, fibrotic scarring develops as a response to ongoing inflammation, manifesting as subepithelial collagen sclerosis and interfollicular hyperplasia that replaces functional lymphoid tissue.^[17] Epithelial metaplasia, including acanthosis and disrupted surface integrity, further compromises the mucosal barrier, reducing immune efficiency by impairing lymphocyte recruitment and antigen presentation.^[14] This fosters an increased risk of persistent low-grade infection, as the altered epithelium allows bacterial adhesion and evasion of clearance mechanisms.^[18] Histologically, chronic changes shift the tonsillar architecture from lymphoid dominance—with prominent germinal centers—to stromal fibrosis, evidenced by enlarged follicles interspersed with fibrous bands and reduced cellularity in reactive states.^[19] Such transformations can lead to obstructive symptoms from mass effect, particularly in hypertrophied tonsils where fibrosis limits tissue compliance.^[20]

Signs and Symptoms

Acute Presentation

Acute tonsillitis typically presents with a sudden onset of sore throat and odynophagia, characterized by painful swallowing that can make eating and drinking difficult.^[2]^[1] Patients often develop a fever ranging from 38°C to 40°C, accompanied by chills, which contributes to the acute discomfort.^[2]^[21] These symptoms generally last 3 to 7 days, with most cases resolving without complications.^[2] On physical examination, the tonsils appear erythematous and swollen, often covered with white or yellow exudate or patches indicating inflammation or infection.^[2]^[1] Tender anterior cervical lymphadenopathy is a common finding, reflecting the localized immune response to the infection.^[2]^[21] Associated features include headache, malaise, and otalgia, which may manifest as referred ear pain due to shared nerve innervation.^[2]^[1] Halitosis often arises from bacterial overgrowth on the inflamed tonsils.^[2] The condition's severity typically peaks within 2 to 3 days, after which symptoms begin to subside.^[2] In viral cases, additional upper respiratory symptoms such as rhinorrhea or cough are frequently present, helping differentiate from bacterial etiologies.^[2]^[1]

Chronic Presentation

Chronic tonsillitis involves persistent, low-grade inflammation of the tonsils over months or longer, distinct from recurrent acute episodes (which are defined by criteria such as at least seven infections in one year, five per year for two years, or three per year for three years). It manifests with subtle, ongoing symptoms rather than discrete acute flares.^[2]^[22] Patients typically experience intermittent throat discomfort, a persistent sensation of a foreign body in the throat, and recurrent low-grade fevers that do not resolve completely between episodes.^[15] These symptoms can lead to chronic fatigue and reduced quality of life due to their protracted nature. In addition, tonsil stones, or tonsilloliths, frequently develop in the tonsillar crypts as calcified debris from food particles, bacteria, and dead cells, resulting in chronic halitosis and a foul taste in the mouth.^[23]^[24] In children, chronic tonsillitis often involves tonsillar hypertrophy, which contributes to obstructive symptoms such as snoring, mouth breathing, and dysphonia (altered voice quality) due to partial airway blockage.^[15] These signs arise from enlarged tonsils impeding normal airflow and vocal resonance, potentially exacerbating sleep disturbances and speech issues over time.^[2]

Causes

Viral Etiologies

Viral infections are the most common cause of tonsillitis, accounting for 70% to 95% of cases.^[2] Among these, adenovirus, Epstein-Barr virus (EBV), and rhinovirus represent the primary pathogens, with adenovirus implicated in approximately 20% of pharyngitis cases during late winter and early spring.^[25] EBV often leads to a mononucleosis-like illness, while rhinovirus is frequently associated with milder upper respiratory symptoms.^[2] Other notable viruses include influenza, parainfluenza, coxsackievirus, and coronaviruses (such as common cold strains excluding SARS-CoV-2).^[2] These agents contribute to the majority of non-bacterial tonsillitis episodes, particularly in children and young adults. Transmission occurs primarily through respiratory droplets or direct contact with contaminated surfaces or secretions.^[1] The incubation period for most viral tonsillitis is typically 2 to 5 days, though it varies by pathogen—adenovirus has an incubation of 5 to 10 days, while EBV requires 4 to 7 weeks.^[2] Infections are generally self-limiting, resolving within 7 to 10 days without specific antiviral treatment.^[2] Distinct clinical features can aid in identifying specific viruses; for instance, EBV-associated tonsillitis often presents with splenomegaly, posterior cervical lymphadenopathy, and a characteristic rash (particularly if ampicillin is administered).^[26] Adenovirus infections may accompany conjunctivitis, reflecting its tropism for ocular and respiratory tissues.^[2]

Bacterial Etiologies

Bacterial etiologies account for approximately 15-30% of acute tonsillitis cases in children and 5-20% in adults, with Streptococcus pyogenes (group A Streptococcus, or GAS) being the predominant pathogen responsible for the majority of these infections.^[27] In adolescents and young adults, Fusobacterium necrophorum emerges as a significant secondary cause, detected in up to 20-27% of symptomatic cases in this age group, often rivaling GAS in prevalence.^[28]^[29] These bacterial agents necessitate targeted diagnostic approaches, such as rapid antigen testing or throat cultures for GAS, due to the potential for severe sequelae if untreated, underscoring the importance of distinguishing bacterial from viral causes in clinical management.^[2] Less common bacterial contributors include Staphylococcus aureus, Haemophilus influenzae, and various anaerobes such as Prevotella and Fusobacterium species (beyond necrophorum), which are frequently identified in mixed infections or recurrent cases.^[2]^[14] These pathogens typically play a supportive role in polymicrobial tonsillar inflammation rather than acting as primary isolates.^[30] Transmission of bacterial tonsillitis primarily occurs through respiratory droplets via close contact, such as in schools, households, or crowded settings, with an incubation period of 2-5 days.^[31]^[32] GAS infections carry risks of both suppurative complications, like peritonsillar abscess, and non-suppurative ones, including acute rheumatic fever, which can affect cardiac valves and joints if the infection progresses unchecked.^[32] F. necrophorum similarly predisposes to suppurative issues, such as Lemierre's syndrome involving jugular vein thrombophlebitis.^[33] Key risk factors for bacterial tonsillitis include poor personal hygiene, household overcrowding, and seasonal patterns peaking in winter months, which facilitate airborne spread in enclosed environments.^[34]^[27] Viral co-infections may occasionally exacerbate bacterial adherence to tonsillar tissue, though bacterial pathogens remain the dominant drivers of treatable disease.^[2]

Diagnosis

Clinical Assessment

The clinical assessment of tonsillitis begins with a detailed history to identify risk factors and guide suspicion for bacterial versus viral etiology. Key elements include the patient's age, as group A Streptococcus (GAS) pharyngitis is most common in children aged 5 to 15 years; frequency of prior episodes, which may indicate recurrent tonsillitis warranting further evaluation; recent exposure to individuals with sore throat or confirmed streptococcal infection; and history of recent antibiotic use, which could influence current presentation or suggest incomplete prior treatment.^[31]^[2] Additional historical features, such as sudden onset of sore throat without associated cough or rhinorrhea, raise suspicion for bacterial causes.^[2] Physical examination focuses on oropharyngeal inspection and cervical palpation to evaluate for inflammatory signs. Throat examination reveals tonsillar erythema, hypertrophy, or purulent exudates, with asymmetry potentially indicating complications like peritonsillar abscess; tonsil size is graded on the Brodsky scale from 0 (tonsils within the tonsillar fossa) to 4 (tonsils occluding >75% of the oropharynx or touching midline).^[2]^[35] Palpation assesses for tender, enlarged anterior cervical lymph nodes, which are suggestive of bacterial infection, while posterior cervical nodes may point to viral etiologies like infectious mononucleosis.^[36] Fever greater than 38°C (100.4°F) is documented, and absence of cough is noted as a distinguishing feature.^[31] Scoring systems such as the Centor criteria aid in estimating the likelihood of GAS pharyngitis based on clinical features alone. The original Centor score assigns 1 point each for fever >38°C, absence of cough, tender anterior cervical lymphadenopathy, and tonsillar exudates or swelling, yielding a total of 0 to 4; scores of 0-1 indicate low likelihood (7-12%), 2-3 moderate (21-38%), and 4 high (57%).^[36] The modified Centor (McIsaac) score adjusts for age by adding +1 point for ages 3-14 years, 0 for 15-44 years, and -1 for ≥45 years, resulting in scores from -1 to 5 with corresponding GAS probabilities of 7.6-13.1% for 0-1, 20.8-33.6% for 2-3, and 50.7-69.3% for 4-5.^[36] These tools help estimate the likelihood of GAS pharyngitis and determine whether laboratory testing is warranted, with low scores indicating a low probability and potentially avoiding unnecessary tests.^[36] Differential considerations during assessment include distinguishing tonsillitis from infectious mononucleosis, which often presents with bilateral tonsillar enlargement, fatigue, and posterior lymphadenopathy in adolescents and young adults, and peritonsillar abscess, identified by unilateral tonsillar asymmetry, trismus, and uvular deviation.^[2]^[37] Thorough inspection for these features ensures appropriate suspicion of alternative or complicating diagnoses.^[2]

Laboratory Tests

Laboratory tests play a crucial role in confirming the etiology of tonsillitis, particularly to distinguish bacterial from viral causes and guide appropriate therapy. According to 2025 IDSA guidelines, routine testing for GAS is not recommended in children under 3 years of age, as the condition is uncommon in this group. Testing is guided by clinical scoring: low scores (e.g., Centor/McIsaac 0-1) suggest viral etiology with no testing needed, while moderate-to-high scores or high-risk patients (e.g., recent exposure, history of rheumatic fever) warrant testing.^[36] The rapid antigen detection test (RADT) for group A Streptococcus (GAS) is a common point-of-care method using a throat swab to detect streptococcal antigens, offering results within minutes. Its sensitivity ranges from 70% to 90%, with specificity exceeding 95%, making it reliable for ruling in GAS infection but less so for ruling it out, especially in children where sensitivity may be lower around 85%.^[38]^[39] Testing via RADT is recommended before initiating antibiotics to avoid false negatives, ideally within the first 24 hours of symptom onset.^[31] Throat culture remains the gold standard for diagnosing bacterial tonsillitis, involving plating a throat swab on blood agar to identify pathogens like GAS, with results typically available in 24 to 48 hours. It is particularly indicated when RADT is negative in high-risk patients or to confirm non-GAS bacteria. For suspected viral causes such as Epstein-Barr virus (EBV) or cytomegalovirus (CMV), polymerase chain reaction (PCR) testing on throat swabs or other samples can detect viral DNA if clinical suspicion is high, though it is not routine.^[31]^[3]^[40] Blood tests provide supportive evidence but are not primary for diagnosis. A complete blood count (CBC) often reveals leukocytosis in bacterial cases, indicating an inflammatory response, while a monospot test (heterophile antibody assay) detects EBV-associated infectious mononucleosis with high specificity in adolescents and adults, yielding results in about an hour. Antistreptolysin O (ASO) titer measures antibodies to streptococcal antigens and is useful for confirming recent GAS infection in cases of post-streptococcal complications, with elevated levels persisting for weeks.^[41]^[42]^[43] Imaging studies, such as ultrasound or computed tomography (CT), are rarely required for uncomplicated tonsillitis diagnosis and have no routine role. They may be employed in select cases to evaluate for peritonsillar abscess, where ultrasound offers a non-invasive bedside option with good sensitivity for fluid collections, or CT provides detailed assessment of deep neck involvement when surgical intervention is considered.^[44]^[45]

Treatment

Supportive Care

Supportive care forms the cornerstone of management for tonsillitis, focusing on symptom relief and promoting natural recovery in both viral and bacterial cases, regardless of etiology.^[46] These measures are particularly important for alleviating the throat pain and discomfort that characterize acute presentations.^[1] Analgesics are a primary component to control pain and fever. Acetaminophen or ibuprofen are commonly recommended, with dosing tailored by age and weight to ensure safety and efficacy. For children, acetaminophen is typically administered at 10-15 mg/kg every 4-6 hours as needed, not exceeding 75 mg/kg per day.^[47] Ibuprofen may be given at 5-10 mg/kg every 6-8 hours, with a maximum of 40 mg/kg per day, and is avoided in infants under 6 months without medical advice.^[48] Aspirin should be avoided in children and adolescents due to the risk of Reye's syndrome.^[3] Hydration, rest, and environmental adjustments support overall recovery by reducing mucosal irritation and preventing complications like dehydration. Patients are encouraged to drink plenty of fluids, such as water or warm broths, to maintain throat moisture and hydration status.^[3] Rest is essential to bolster immune function, while a soft diet of easily swallowable foods like soups or yogurt minimizes discomfort during swallowing. Using a cool-mist humidifier or inhaling steam from a warm shower can further soothe inflamed tissues by adding moisture to the air.^[49] Local therapies provide targeted relief for throat soreness. Throat lozenges containing menthol or benzocaine are suitable for children over 4 years to ease pain, while saltwater gargles—prepared by dissolving 1/2 teaspoon of salt in 8 ounces of warm water—can reduce inflammation when patients are able to gargle and spit.^[3] Topical anesthetics, such as sprays with lidocaine, may also be used under medical guidance for short-term numbing.^[46] For mild tonsillitis, home-based supportive care suffices, but vigilant monitoring is crucial. Caregivers should watch for signs of dehydration (e.g., reduced urine output, dry mouth) or breathing difficulties (e.g., stridor, rapid breathing), and seek immediate medical evaluation if these or other worsening symptoms like high fever or inability to swallow occur.^[1]

Antimicrobial Therapy

Antimicrobial therapy for tonsillitis is reserved for cases confirmed or highly suspected to be bacterial, primarily due to group A beta-hemolytic Streptococcus (GABHS), also known as Streptococcus pyogenes. Antibiotics are indicated when the modified Centor score is 3 or greater, suggesting a higher pretest probability of GABHS infection, or when rapid antigen detection testing (RADT) or throat culture confirms the presence of GABHS.^[2]^[50] Routine antimicrobial use is not recommended for viral tonsillitis, as it does not improve outcomes and promotes resistance.^[31] The first-line treatment for confirmed GABHS tonsillitis is penicillin V or amoxicillin, both of which exhibit excellent efficacy against susceptible strains with minimal resistance reported globally. For adults, penicillin V is dosed at 250 to 500 mg orally two to three times daily for 10 days; for children, the dose is 250 mg two to three times daily.^[31]^[2] Amoxicillin offers a convenient alternative, administered as 50 mg/kg once daily (maximum 1,000 mg) for 10 days in children or 500 mg twice daily in adults, providing comparable bacteriological cure rates of over 90%.^[31]^[46] This 10-day duration ensures eradication of GABHS from the pharynx and reduces the risk of suppurative complications, such as peritonsillar abscess, by approximately 50% compared to shorter courses.^[36] In patients with penicillin allergy, alternative agents include azithromycin or clindamycin, selected based on local resistance patterns and allergy severity. Azithromycin is given as 12 mg/kg once daily (maximum 500 mg) for 5 days in children or 500 mg on day 1 followed by 250 mg daily for 4 days in adults, while clindamycin is dosed at 20 mg/kg daily in three divided doses (maximum 600 mg/day) for 10 days.^[31]^[46] Cephalexin, a first-generation cephalosporin, may be used for non-anaphylactic allergies at 20 mg/kg twice daily (maximum 500 mg/dose) for 10 days, though cross-reactivity risks must be weighed.^[31] Resistance to macrolides, such as azithromycin, in GABHS has been rising in certain regions, with rates varying from approximately 5-10% in North America to over 20% in some European countries (e.g., Italy and Spain), as of 2024, necessitating vigilance and potential culture-guided therapy in areas of high prevalence.^[51] Penicillin resistance remains virtually absent, reinforcing its status as the cornerstone of therapy.^[36] For patients with recurrent GABHS tonsillitis, particularly those at high risk for rheumatic fever or with multiple episodes (e.g., three or more per year), secondary prophylaxis with intramuscular benzathine penicillin G is recommended. This involves 1.2 million units administered every 3 to 4 weeks, typically for at least 5 years or until age 21, whichever is longer, to prevent reinfection and associated sequelae.^[52]^[53] Such regimens have demonstrated over 90% effectiveness in reducing recurrence rates in high-risk populations.^[54]

Surgical Interventions

Surgical interventions for tonsillitis primarily involve tonsillectomy, the surgical removal of the palatine tonsils, reserved for cases of recurrent or complicated disease that do not respond adequately to conservative management.^[55] Indications for tonsillectomy are guided by the Paradise criteria, established in a landmark randomized controlled trial, which recommend surgery for children with a history of at least seven documented episodes of throat infection in the preceding year, five episodes per year for two years, or three episodes per year for three years, where each episode includes fever, cervical adenopathy, tonsillar exudate, or positive streptococcal testing.^[56] These criteria emphasize well-documented, frequent, and debilitating infections to ensure benefits outweigh surgical risks.^[22] The standard procedure for complete tonsillectomy involves extracapsular dissection, where the tonsils are fully removed along with their capsules, typically using cold steel dissection with snare or scissors for tissue separation and hemostasis achieved via ties, cautery, or sutures.^[57] An alternative technique is coblation tonsillectomy, which employs low-temperature radiofrequency energy to dissolve tissue in a plasma field, allowing precise dissection with reduced thermal injury to surrounding structures and potentially less postoperative pain.^[57] Both methods are performed under general anesthesia as outpatient procedures in most cases, with operative time averaging 20-30 minutes per side.^[58] In children with tonsillitis complicated by obstructive sleep apnea (OSA), partial tonsillectomy (tonsillotomy) may be considered, preserving tonsillar tissue to minimize risks while alleviating airway obstruction; this approach has shown comparable efficacy to total tonsillectomy in improving sleep-disordered breathing outcomes.^[59] If adenoidal hypertrophy contributes to obstruction, adenotonsillectomy—combining partial or total tonsillectomy with adenoidectomy—is indicated, particularly when polysomnography confirms moderate to severe OSA.^[60] Risks of tonsillectomy include postoperative hemorrhage, occurring in 1-3% of cases, with primary bleeding (within 24 hours) at 0.2-2% and secondary bleeding (after 24 hours) at 0.1-3%, often requiring return to the operating room in severe instances; infection risk is lower, around 1%, typically managed with antibiotics.^[61] Benefits include a significant reduction in the frequency and severity of throat infection episodes, with randomized trials demonstrating approximately 50% fewer sore throat days over two years compared to conservative management, alongside improvements in quality of life.^[62] The 2019 update to the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) clinical practice guideline reinforces these indications while prioritizing shared decision-making, urging clinicians to discuss episode frequency, symptom impact on daily activities, and patient-specific factors like age and comorbidities to tailor recommendations and enhance informed consent.^[55]

Complications and Prognosis

Potential Complications

Tonsillitis can lead to various local and systemic complications if untreated or severe, primarily arising from bacterial spread or immune responses. Local complications include suppurative infections adjacent to the tonsils. Peritonsillar abscess, a collection of pus in the space surrounding the tonsil, develops as a complication of acute bacterial tonsillitis in approximately 1% of cases and typically requires surgical drainage along with antibiotics.^[63] Otitis media and sinusitis may also occur due to contiguous spread of infection from the pharynx, affecting the middle ear or paranasal sinuses, respectively, and are reported in about 1% of sore throat episodes overall.^[63] Systemic complications are more commonly associated with group A Streptococcus (GAS) infections. Acute rheumatic fever, an autoimmune sequela, arises in 0.3-3% of untreated GAS pharyngitis cases, potentially leading to carditis or joint inflammation.^[64] Post-streptococcal glomerulonephritis, involving immune-mediated kidney inflammation, follows GAS tonsillitis in a small fraction of cases, with incidence varying by strain but generally low in developed settings at around 5-10% for nephritogenic strains.^[65] Scarlet fever, characterized by a diffuse rash from streptococcal pyrogenic exotoxins, complicates approximately 10% of GAS pharyngitis episodes but is now rare due to immunity and treatment. However, as of 2025, there have been reported increases in scarlet fever and invasive GAS infections in multiple countries, including Europe, Asia, and North America.^[66]^[67] Rare complications include Lemierre's syndrome, a septic thrombophlebitis of the internal jugular vein often caused by Fusobacterium necrophorum in adolescent tonsillitis, with an estimated incidence of 1 case per 1,000,000 population annually.^[68] Severe tonsillar edema can also cause airway obstruction, necessitating urgent intervention in critical cases.

Long-term Outlook

For acute cases of tonsillitis, approximately 90% resolve without long-term sequelae within 1 to 2 weeks, primarily through supportive care for viral etiologies and antibiotics for bacterial infections.^[2] Viral tonsillitis typically improves in 7 to 10 days, while bacterial cases, such as those caused by group A Streptococcus, show symptom resolution in about 10 days with appropriate antimicrobial therapy.^[69] Without intervention beyond initial treatment, recurrence occurs in 20% to 30% of cases, often defined as multiple episodes per year, leading to potential impacts on daily activities and school absences.^[46] In chronic or recurrent tonsillitis, tonsillectomy significantly improves outcomes, reducing episode frequency by more than 70% in the first postoperative year and sustaining benefits over time.^[70] For instance, patients experience a drop from an average of 6 to 7 episodes annually pre-surgery to 1 to 2 thereafter, enhancing quality of life through decreased antibiotic use and fewer healthcare visits.^[70] Long-term immune function remains unaffected, with studies showing no significant negative impact on humoral or cellular immunity years after the procedure.^[71] Mortality from tonsillitis is near zero, at less than 0.01%, in developed settings due to timely access to antibiotics and supportive care that prevents suppurative and nonsuppurative complications.^[2] In low-resource areas, however, mortality is higher owing to delayed treatment and increased risk of severe complications like rheumatic fever or peritonsillar abscess.^[2] Follow-up care should include monitoring for post-streptococcal autoimmune issues, such as acute rheumatic fever, for up to 3 to 4 weeks after symptom onset, with clinical assessment for carditis or arthritis if symptoms persist.^[72]

Epidemiology

Incidence and Prevalence

Tonsillitis is a prevalent condition, accounting for approximately 1.3% of all outpatient visits worldwide.^[2] In the United States, it represents about 2% of ambulatory encounters.^[2] The annual incidence of acute tonsillitis or sore throat in school-aged children is approximately 100–200 cases per 1,000 population.^[2] Of these cases in the US and Europe, 15% to 30% are bacterial, predominantly caused by Group A Streptococcus, while the majority (70% to 85%) are viral.^[2] The condition is rare in children under 2 years of age, peaks between 5 and 15 years, and incidence declines markedly after age 25.^[2] Prevalence is elevated in temperate climates, where cases surge during winter and early spring months due to increased viral transmission.^[2] Globally, the burden among children is significant, with an estimated 288.6 million episodes of Group A Streptococcus-associated sore throat occurring annually in those aged 5 to 14 years (as of 2016).^[73] Incidence rates are notably higher in developing countries, where overcrowding and poor living conditions exacerbate transmission, as highlighted in assessments of related streptococcal diseases.^[74]

Risk Factors

Tonsillitis risk is influenced by both non-modifiable and modifiable factors that predispose individuals to infection or recurrent episodes. Non-modifiable factors include age, particularly between 5 and 15 years, when the condition is most prevalent due to immature immune systems and higher exposure in school settings.^[1] Family history also plays a significant role, with genetic effects accounting for approximately 62% of the variation in recurrent tonsillitis liability, suggesting inherited susceptibility to chronic inflammation or immune dysregulation.^[75] Modifiable risk factors encompass environmental and behavioral elements that heighten exposure to infectious agents. Attendance at daycare or preschool facilities elevates risk through frequent close contact with peers carrying respiratory viruses or bacteria, facilitating transmission in crowded environments.^[69] Exposure to passive smoking irritates the respiratory tract and impairs mucosal defenses, increasing susceptibility to tonsillitis in children by promoting bacterial adherence and inflammation.^[76] Low socioeconomic status correlates with higher incidence, often due to overcrowded living conditions, limited access to healthcare, and poorer hygiene practices that amplify pathogen spread.^[77] Seasonal exposure to viruses, particularly during winter months when indoor gatherings and lower humidity favor viral survival, further contributes to outbreaks of viral tonsillitis.^[78] Comorbidities can exacerbate tonsillitis risk by underlying immune vulnerabilities. Immunodeficiencies, such as those seen in HIV infection, compromise T-cell function and mucosal immunity, leading to more frequent and severe tonsillar infections as opportunistic pathogens exploit weakened defenses.^[79] Allergies may worsen inflammation by triggering postnasal drip and chronic irritation of the tonsils, creating an environment conducive to secondary bacterial overgrowth and acute episodes.^[80] Recent studies from the COVID-19 era (2020-2023) highlight the impact of public health measures on tonsillitis incidence, with widespread masking and social distancing linked to significant reductions in cases, particularly among children, due to decreased viral transmission in community settings. Post-2023 data suggest a partial rebound in cases as measures were relaxed.^[81]

Prevention

Hygiene and Lifestyle Measures

Practicing good hygiene is essential for reducing the risk of tonsillitis, which is primarily caused by bacterial or viral pathogens transmitted through respiratory droplets or direct contact.^[82]^[83] Frequent handwashing with soap and water for at least 20 seconds, particularly after contact with individuals who are ill or touching shared surfaces, helps eliminate pathogens and prevents their transfer to the mouth or nose. Avoiding the sharing of utensils, drinking glasses, or other personal items further minimizes direct transmission of bacteria like group A Streptococcus.^[83]^[84] Adhering to respiratory etiquette, such as covering the mouth and nose with a tissue or elbow when coughing or sneezing, and disposing of tissues immediately, limits the spread of infectious droplets. Individuals experiencing symptoms of tonsillitis should stay home from work, school, or social activities to avoid exposing others until they are no longer contagious, typically after 24 hours of antibiotic treatment for bacterial cases.^[83]^[84] Maintaining a moist indoor environment with a clean cool-mist humidifier can help preserve the moisture of throat and nasal mucosa, potentially reducing susceptibility to irritation and infection. Avoiding exposure to environmental irritants, including cigarette smoke and secondhand smoke, is crucial, as these can inflame the throat lining and impair local immune defenses.^[3]^[49]^[84] Staying well-hydrated supports overall immune function by aiding in the maintenance of mucosal barriers in the respiratory tract. Consuming foods rich in vitamin C, such as citrus fruits, may provide general immune support through its antioxidant properties and role in enhancing white blood cell activity, though it has not been proven to directly prevent tonsillitis.^[85]

Vaccination and Prophylaxis

There is no vaccine specifically targeting tonsillitis itself, as it is typically caused by a range of viral and bacterial pathogens rather than a single agent. However, certain vaccines can indirectly reduce the incidence of tonsillitis by preventing infections that commonly lead to or complicate tonsillar inflammation. The influenza vaccine is recommended annually for all individuals aged 6 months and older to mitigate viral respiratory infections, which account for the majority of acute tonsillitis cases and can predispose patients to secondary bacterial superinfections in the tonsils.^[86] Similarly, pneumococcal conjugate vaccines (such as PCV15 or PCV20) are advised for children under 5 years and high-risk adults to prevent Streptococcus pneumoniae infections, which can cause bacterial tonsillitis and reduce the overall burden of upper respiratory tract complications.^[87]^[88] For bacterial tonsillitis primarily caused by group A beta-hemolytic Streptococcus (GABHS), no licensed vaccine exists as of November 2025. Several candidates are in clinical trials, including multivalent M protein-based and peptide-conjugate formulations.^[89]^[90] Antibiotic prophylaxis is not routinely recommended for preventing recurrent GABHS tonsillitis due to risks of antimicrobial resistance; tonsillectomy is preferred for severe recurrent cases meeting established criteria. Prophylaxis with antibiotics such as intramuscular benzathine penicillin may be considered specifically for secondary prevention of acute rheumatic fever in patients with a history of it.^[91] For high-risk children, such as those with underlying conditions increasing susceptibility to respiratory infections, annual influenza vaccination is particularly emphasized to lower the likelihood of influenza-associated tonsillitis exacerbations.^[92]

History and Society

Historical Perspectives

Tonsillitis, recognized in ancient times as an inflammatory condition of the throat, was first described by the Greek physician Hippocrates in the 5th century BCE, who referred to severe cases involving peritonsillar abscess as "quinsy," noting symptoms such as swelling, pain, and the need for incision and drainage.^[93] This early account highlighted quinsy as a potentially life-threatening complication of throat infections, distinguishing it from milder inflammations, and laid foundational observations on its clinical presentation that persisted into later medical texts.^[94] In the 19th century, medical understanding advanced with connections drawn between tonsillitis and systemic diseases, particularly by French physicians in the 1880s who linked recurrent throat infections to rheumatic fever, emphasizing the role of streptococcal bacteria in precipitating joint and cardiac complications.^[95] This association, building on earlier 17th-century descriptions of acute rheumatism, underscored tonsillitis as a focal point for infection that could disseminate, influencing diagnostic and preventive approaches.^[96] Surgical interventions for tonsillitis trace back to the Roman physician Aulus Cornelius Celsus around 50 CE, who documented the first known partial tonsillectomy using digital extraction or a blunt hook to remove enlarged tonsils, followed by rinses with vinegar to reduce inflammation.^[97] This rudimentary procedure targeted symptomatic relief in cases of obstruction or severe inflammation, marking an early milestone in otolaryngologic surgery. The modern technique of complete tonsillectomy emerged in 1889, when Danish surgeon Wilhelm Meyer introduced dissection using a blunt dissector, enabling more thorough removal and reducing recurrence risks compared to prior partial methods.^[98] The 20th century brought significant shifts in tonsillitis management, with routine tonsillectomies peaking in the 1950s—reaching 1.4 million procedures annually in the United States—driven by beliefs in preventing recurrent infections and related conditions like rheumatic fever under the focal infection theory.^[99] However, post-1940s antibiotic therapies, particularly penicillin, dramatically reduced the severity and complications of bacterial tonsillitis, curbing the need for prophylactic surgery.^[100] By 1984, randomized trials established evidence-based criteria for tonsillectomy, limiting it to children with severe, recurrent infections (at least seven episodes in the prior year, five annually for two years, or three annually for three years, each with documentation of fever, cervical adenopathy, or positive cultures), thereby declining overuse and emphasizing conservative management.^[101] In twentieth-century Britain, attitudes toward tonsillitis treatment underwent significant cultural shifts, particularly regarding tonsillectomy. Early in the century, the procedure was widely embraced as a preventive measure against infections and social ills like physical deterioration, with over 80,000 schoolchildren undergoing it annually by 1927, supported by state health initiatives.^[102] By mid-century, concerns over complications such as bulbar poliomyelitis led to public skepticism and declining rates, while later decades saw criticism of it as a "dangerous fad" due to psychological impacts on children and rising healthcare costs, influencing stricter surgical guidelines.^[102] Traditional remedies remain integral to cultural practices in many regions. In Ethiopia, 51 medicinal plant species from 31 families are used to treat tonsillitis, with Rhamnus prinoides and Zingiber officinale being the most common; leaves and roots are typically chewed or prepared fresh for oral administration, driven by sociocultural beliefs in their efficacy and local availability.^[103] Among Arabic and Muslim communities in the United Arab Emirates, honey—often mixed with lemon—is viewed as a "magic cure" for tonsillitis and sore throat, rooted in religious texts like the Quran that endorse its healing properties, though this can delay biomedical care.^[104] In The Gambia, sore throats (frequently encompassing tonsillitis) are initially managed at home with remedies like black pepper in hot water, influenced by beliefs that the condition stems from poor hygiene or spicy foods rather than bacterial causes, leading to preferences for traditional over formal medicine.^[105] Socially, tonsillitis imposes burdens on families and communities, particularly affecting children. Recurrent episodes cause school absences, parental work disruptions, and emotional strain, with parents reporting heightened worry linked to episode duration and severity.^[106]^[107] Low socioeconomic status correlates with higher childhood incidence in regions like Somalia, exacerbating access to care and perpetuating cycles of infection through overcrowding and poor hygiene.^[108] Racial and ethnic disparities in treatment are evident in the United States, where Black children undergo tonsillectomy at lower rates than White children, potentially due to barriers in ambulatory surgery access and healthcare inequities.^[109] Public health measures like social distancing during the COVID-19 pandemic demonstrated tonsillitis's sensitivity to social behaviors, with Denmark reporting a 57% drop in the incidence of severe acute tonsillitis cases referred to hospitals, attributed to reduced transmission in schools and households.^[110] Following the lifting of restrictions, incidence rebounded, with notable increases in group A Streptococcus pharyngitis cases—a common cause of bacterial tonsillitis—in 2023 and 2024.^[111] Overall, these cultural and social dimensions highlight how tonsillitis intersects with societal structures, influencing both prevention strategies and quality of life.

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[110]
Recurrent tonsillitis and parental perceptions of tonsillectomy during ...
Oct 23, 2020 · We aimed to investigate the impact on patients with recurrent tonsillitis and parental perceptions towards tonsillectomy during the COVID-19 pandemic.
[111]
Factors Associated with Childhood Tonsillitis in Somalia
Conclusion: Low socioeconomic status, family history of tonsillitis, and poor personal hygiene were all associated with childhood tonsillitis.
[112]
The impact of social restrictions on the incidence and microbiology ...
Sep 10, 2024 · The aims of the present study were to explore the impact of social restriction on 1) the incidence, 2) the severity of illness and 3) the bacterial findings of ...