Tonsillitis is a common illness that requires a careful clinical assessment in order to identify underlying etiology and to avoid morbidity and mortality.
Case Presentation
A previously healthy 35-year-old man with history of appendectomy, bilateral inguinal hernia repair, lumbar laminectomy, chronic low back pain, opiod dependence, and recurrent tonsillitis presented with 2-day history of headache, high fever and chills, painful deglutition, inability to swallow solids, and lower abdominal pain in May this year. He denied rash, nasal discharge, cough, muscle aches, joint pains, nausea, vomiting, diarrhea, and urinary symptoms.
Assessment
On examination he was tall, well nourished, moderately ill, and tachycardic due to fever of 38.3°C. Physical examination revealed orthopnea, bilateral tender jugulodigastric lymphadenopathy, trismus, odynophagia, pooling of saliva, pharyngeal congestion, erythematous uvula, soft palate erythema, and bilaterally enlarged tonsils covered with white exudates (Figure, A and B). Routine laboratory tests showed polymorphonuclear leukocytosis and negative monospot test. Soft tissue radiograph and magnetic resonance imaging study of the neck revealed prominent tonsillar pillars and tonsillar enlargement (peritonsillitis). Tonsillar exudate culture confirmed beta-hemolytic group A streptococcal tonsillitis. Differential diagnosis includes beta-hemolytic streptococci (Lancefield groups B, C, and G), Epstein-Barr virus, adenovirus, Fusobacteria, Arcanobacterium hemolyticum, Corynebacterium diphtheriae, C. ulcerans, Francisella tularensis, Yersinia entercolitica, and Neisseria gonorrhea. Streptococcal exudative lesions are seen as milk white or gray scum (follicles), which can be removed without bleeding. Such follicular exudates coalesce if untreated and mimic a “pseudomembrane.” Others produce a gray-white tightly adherent layer that can be removed, leaving the underlying surface bleeding (pseudomembrane).
Epstein-Barr virus, the most common cause of pseudomembranous tonsillitis, causes tonsillitis with or without infectious mononucleosis.(1) The tonsils can be severely enlarged and are covered with an extensive necrotic, grayish-white membranous exudate. Infectious mononucleosis usually causes fever, sore throat, periorbital and upper eyelid edema (Hoagland’s sign), palatal petechiae, erythematous or exudative tonsillitis, bilateral posterior cervical lymphadenopathy, hepatosplenomegaly, ampicillin rash, and Gianotti-Crosti syndrome. Corynebacterium diphtheria, C. pseudodephtheria, and C. ulcerans produce gray-white, sharply demarcated pseudomembrane consisting of inflammatory cells, red cells, and necrotic tonsillar epithelial layer in a network of fibrin adherent to underlying tissue, and removal would result in bleeding.(2) Unlike Epstein-Barr virus, diphtheria pseudomemrane can involve the uvula and soft palate. Other features are anterior and submandibular cervical lymphadenopathy (bull’s neck), cardiorespiratory insufficiency, and neurologic dysfunction due to diphtheria toxin. Arcanobacterium haemolyticum tonsillitis in college students is often accompanied by scarlatiniform rash. Adenovirus tonsillitis, seen usually in public swimming pools and in military recruits, causes coryza, influenza-like illness, gastroenteritis, kerato-conjunctivitis, tonsillar pseudomembrane formation due to necrosis of superficial layer of tonsil, and pharyngoconjunctival fever. Herpes simplex tonsillitis often follows herpes labialis and gingivostomatitis. The exudative lesions are accompanied by vesicles and ulcerations. Gonococcal tonsillitis, with whitish-yellow tonsillar exudates with gingivostomatitis, is seen in sexually active patients. Anaerobic tonsillitis (Vincent angina) due to Fusobacterium necrophorum presents as gingivostomatitis, ulceration, pseudomembranous exudate, and fetid odor. Oropharyngeal infection may spread to underlying carotid sheath, causing suppurative thrombophlebitis and metastasis (Lemierre syndrome).
Diagnosis
Beta hemolytic Group A streptococci is the most common cause of acute tonsillitis. Tonsillitis with tender anterior cervical lymphadenitis in a person with a recent history of exposure to streptococcal tonsillitis is highly suggestive of streptococcal group A etiology.(3) Streptococcal tonsillitis, common in winter and early spring, is manifested as acute onset of fever, headache, neck pain, odynophagia, otalgia, sore throat, sour-sweet yeasty odor, nausea, vomiting, abdominal pain, flushed cheeks, red tongue with enlargement of the papillae (“strawberry tongue”), beefy red swollen uvula, soft palatal petechiae (“doughnut” lesions), erythematous, follicular, tender anterior cervical adenitis, scarlet fever rash (due to erythrogenic toxin causing punctate red macules in proximal extremities, accentuated on flexor creases—“Pastia’s lines”), circumoral pallor, peritonsilitis (peritonsillar cellulitis), peritonsillar and retropharyngeal abscess, mediastinitis, pneumonia, septicemia, toxic shock syndrome, acute rheumatic fever, poststreptococcal glomerulonephritis, and PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections).
It is necessary to distinguish between tonsillitis and peritonsillar abscess by clinical examination, ultrasound, computed tomography scan or, preferably, magnetic resonance imaging of the neck. Peritonsillar abscess is often confused with severe exudative tonsillitis. In tonsillitis, tonsils, and not the pillars, are enlarged. Peritonsillar abscess, the most common complication of acute tonsillitis, is characterized by accumulation of pus between the tonsil and its capsule. Clinical features include muffled voice (“hot potato voice”), trismus (inter-incisor distance is usually
Treatment
The primary antibiotic treatment for acute streptococcal tonsillitis consists of amoxicillin for 10 days to prevent recurrence, rheumatic fever, and glomerulonephritis. In penicillin-allergic patients, macrolide or clindamycin may be tried. Sometimes, even though streptococcus is sensitive to penicillin, adequate clinical improvement might not be seen. This is due to paradoxically reduced bactericidal activities at high drug concentrations, overwhelming number of organisms, presence of tissue beta-lactamase produced by organisms like Staphylococcus aureus, lack of protective alpha-hemolytic streptococci (co-pathogens), and loss of penicillin-binding protein expression (“Eagle effect”).(4, 5) Hence, if no response is evident within 48 hours of penicillin therapy, there was recent antibiotic exposure, there are high penicillin failure rates in the community, or in the presence of comorbidities, then Ampicillin/Sulbactum or Amoxicillin-Clavulanate, or cephalosporin with or without clindamycin may be used. Recurrent streptococcal tonsillitis may be treated with clindamycin, Amoxicillin-Clavulanate, amoxicillin plus rifampin, or macrolide plus metronidazole. Tonsillectomy is indicated in patients with recurrent tonsillitis and failure of medical treatment involving 6-7 episodes of acute tonsillitis in 1 year, 5 episodes per year for 2 consecutive years, or 3 episodes per year for 3 consecutive years, or cardiac valvular disease. Treatment for peritonsillar abscess is drainage of abscess through needle or incision.(6) Quinsy tonsillectomy is usually avoided because of anesthesia risk, bleeding, pain, nasopharyngeal stenosis, and even death. In case of peritonsillar abscess or enlarged tonsils obstructing airway, use of steroid is beneficial.(7, 8)
Acute exudative tonsillitis involves a number of causative pathogens and a wide spectrum of severity. A meticulous clinical examination would differentiate between the 2 most common causes, streptococcus and Epstein-Barr virus. Our patient with streptococcal tonsillitis was successfully treated with piperacillin/tazobactam and hydrocortisone.
— Nilesh N. Patel, MD, Devesh N. Patel, MD
References
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4. Eagle H. Experimental approach to the problem of treatment failure with penicillin (I. Group A streptococcal infection in mice). Am J Med. 1952;13(4):389–399. Abstract | Full-Text PDF (1068 KB) | MEDLINE | CrossRef
5. Brook I. Overcoming penicillin failures in the treatment of Group A streptococcal pharyngo-tonsillitis. Int J Pediatr Otorhinolaryngol. 2007;71(10):1501–1508. Abstract | Full Text | Full-Text PDF (152 KB) | CrossRef
6. Steyer TE. Peritonsillar abscess: diagnosis and treatment. Am Fam Physician. 2002;65(1):93–96.
7. Ozbek C, Aygenc E. Use of steroids in the treatment of peritonsillar abscess. J Laryngol Otol. 2004;118(6):439–442. MEDLINE
8. McGee S, Hirschmann J. Use of corticosteroids in treating infectious diseases. Arch Intern Med. 2008;168(10):1034–1046. CrossRef
Figure (A) Streptococcal tonsillitis: white exudate on swollen tonsil.
Figure(B) Streptococcal tonsillitis: the classic finding is the presence of white follicular exudates. Soft palatal erythema also is present.
This article originally appeared in the January 2009 issue of The American Journal of Medicine.
