Tonsilitis Akut

01Pathophysiology

Acute tonsillitis is an inflammatory process of the palatine tonsils, which are lymphoid tissue masses positioned at the junction of the oral cavity and oropharynx. These tonsils form part of Waldeyer's ring, a circumferential band of lymphoid tissue that serves as a first-line immunologic barrier against inhaled and ingested pathogens.

In viral tonsillitis, the offending organism invades the tonsillar epithelium and triggers a local immune response dominated by lymphocytic infiltration. This produces diffuse pharyngeal erythema, mild tonsillar enlargement, and symptoms that overlap with a typical upper respiratory infection (cough, rhinorrhea, conjunctivitis). The presence of these concurrent symptoms is a key reason why viral etiology does not warrant antibiotic therapy and is a commonly tested concept.

In bacterial tonsillitis caused by GAS (Streptococcus pyogenes), the pathophysiology is driven by bacterial adherence to the tonsillar epithelium via M protein and lipoteichoic acid. The M protein is also the key virulence factor that enables the organism to resist phagocytosis. GAS then releases streptolysin O and S, DNases, and hyaluronidase, which cause direct tissue destruction and a robust neutrophilic inflammatory response. This is why GAS tonsillitis characteristically produces purulent tonsillar exudate and prominent tender anterior cervical lymphadenopathy, unlike most viral causes.

The reason we treat GAS tonsillitis with antibiotics is not primarily to shorten symptom duration (though it does by roughly 1-2 days). The primary goal is to prevent acute rheumatic fever (ARF), a nonsuppurative complication driven by molecular mimicry between the streptococcal M protein and cardiac myosin. This cross-reactivity leads to pancarditis. Antibiotics must be initiated within 9 days of symptom onset to effectively prevent ARF. Notably, antibiotic treatment does not reliably prevent post-streptococcal glomerulonephritis (PSGN), which is mediated by immune complex deposition and follows a different immunologic timeline. This distinction is heavily tested.

02Classification and Clinical Manifestation

Clinical Scoring: Modified Centor (McIsaac) Criteria

Interpretation

03Diagnostic Workup

The diagnostic approach begins with clinical assessment using the Modified Centor score. For patients scoring 2-3, proceed with RADT. If the RADT is positive, the diagnosis is confirmed and you initiate antibiotics. If the RADT is negative in a child or adolescent, you must follow up with a throat culture because the sensitivity of RADT is not high enough to rule out GAS in this age group. In adults, a negative RADT alone is generally sufficient to withhold antibiotics, because adults have a lower risk of ARF and lower GAS prevalence.

A common exam scenario presents a child with classic GAS features but a negative RADT. The correct next step is throat culture, not empirical antibiotics. Conversely, if the question gives you a positive RADT, no further testing is needed regardless of age.

ASO titers should never be ordered in the acute setting. They rise 1-3 weeks after infection and peak at 3-5 weeks. Their role is limited to supporting the diagnosis of ARF or PSGN in a patient with a compatible clinical picture weeks after the pharyngitis episode.

If the vignette describes an adolescent with prolonged sore throat, fatigue, posterior cervical lymphadenopathy, and splenomegaly, pivot to ordering a Monospot test. If the patient is under 4 years old with a similar picture, Monospot may be falsely negative, and EBV-VCA IgM serology becomes the preferred test.

04Management and Treatment

Acute stabilization in GAS tonsillitis centers on prompt antibiotic initiation. Amoxicillin is preferred over penicillin V in children because of its better taste and availability as a palatable suspension, with equivalent efficacy. The full 10-day course is mandatory to eradicate the organism from the pharynx and prevent ARF, even if symptoms resolve within 2-3 days. This is a frequently tested point: a vignette may ask about a patient who feels better at day 3 and asks whether to stop antibiotics. The answer is always to complete the full course.

When adherence is questionable (e.g., a vignette describing a patient with a history of medication noncompliance, or a socially unstable situation), single-dose intramuscular Benzathine Penicillin G is the best choice. This guarantees adequate drug levels without relying on the patient to finish an oral course.

For patients with penicillin allergy, the next step depends on the severity of the allergy. A history of mild rash (non-anaphylactic) allows the use of a first-generation cephalosporin like cephalexin, since the cross-reactivity rate between penicillins and first-generation cephalosporins is low (approximately 1-2%). A history of anaphylaxis, angioedema, or urticaria to penicillin mandates avoidance of all beta-lactams, and the correct choice becomes azithromycin or clindamycin.

Corticosteroids (single-dose dexamethasone) may be used as adjunctive therapy for severe odynophagia to reduce pain and allow oral intake, but this is not the primary treatment and is not universally recommended.

For recurrent tonsillitis, the question often tests whether you know the Paradise criteria for tonsillectomy. If a vignette describes a child meeting these frequency thresholds despite adequate antibiotic courses, the next best step is referral for tonsillectomy.

Peritonsillar abscess is the most common suppurative complication. It presents with severe unilateral sore throat, trismus (difficulty opening the mouth), "hot potato" (muffled) voice, and uvular deviation away from the affected side. Management is needle aspiration or incision and drainage plus IV antibiotics (ampicillin-sulbactam or clindamycin). This must not be confused with uncomplicated tonsillitis.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on tonsillitis questions is by failing to distinguish viral from bacterial etiology. A vignette that includes cough, rhinorrhea, or conjunctivitis alongside sore throat is pointing you toward a viral cause, and the correct answer is supportive care only, not antibiotics. The absence of cough is one of the strongest individual predictors of GAS and is almost always included in well-written GAS vignettes as a deliberate signal.

The second major trap involves EBV mononucleosis. When a vignette describes an adolescent with sore throat and the physician prescribes amoxicillin empirically, followed by the development of a diffuse maculopapular rash, the question is testing your knowledge that aminopenicillins trigger this characteristic rash in EBV infection. The rash is not a true penicillin allergy and should not be documented as one.

A third commonly tested concept is the workup sequence after a negative RADT in a child. Many students incorrectly jump to empirical antibiotics. The correct next step is always throat culture in pediatric patients to avoid missing GAS due to the limited sensitivity of RADT.

Finally, never confuse the nonsuppurative complications. Antibiotics prevent ARF but do not prevent PSGN. Both can appear in the same question stem, and the tested concept is knowing which complication is preventable with timely treatment. The core competency here is recognizing the appropriate clinical scenario, applying the Centor criteria correctly, ordering the right test at the right time, and understanding the rationale for a full antibiotic course: prevention of rheumatic heart disease.