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Acute Exudative Tonsillitis

MAY 19, 2009

4 COMMENTS

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 38.3C. 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 (Hoaglands 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 EpsteinBarr virus, diphtheria pseudomemrane can involve the uvula and soft palate. Other
features are anterior and submandibular cervical lymphadenopathy (bulls 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, keratoconjunctivitis, 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 creasesPastias 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 penicillinallergic 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

1. Yoda K, Sata T, Kurata T, Aramaki H. Oropharyngotonsillitis associated with


nonprimary Epstein-Barr virus infection. Arch Otolaryngol Head Neck Surg.
2000;126(2):185193. MEDLINE
2. Bishai BR, Murphy JR. Diphtheria and other infections caused by Corynebacteria and
related species. In: Kasper DL editors. Harrisons Principles of Internal Medicine. 17th
edn.. New York: McGraw-Hill; 2008;p. 890895.
3. Ebell MH, Smith MA. Does this patient have strep throat?. JAMA. 2000;284(22):2912
2918. MEDLINE | CrossRef
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):389399. Abstract | FullText 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):15011508. Abstract |
Full Text | Full-Text PDF (152 KB) | CrossRef
6. Steyer TE. Peritonsillar abscess: diagnosis and treatment. Am Fam Physician.
2002;65(1):9396.
7. Ozbek C, Aygenc E. Use of steroids in the treatment of peritonsillar abscess. J
Laryngol Otol. 2004;118(6):439442. MEDLINE
8. McGee S, Hirschmann J. Use of corticosteroids in treating infectious diseases. Arch
Intern Med. 2008;168(10):10341046. 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.
http://amjmed.org/acute-exudative-tonsillitis/

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