Updated: Oct 21, 2009
Pharyngitis is a leading cause of pediatric ambulatory care visits. Examination of patients who present with sore throat may reveal tonsillitis, tonsillopharyngitis, or nasopharyngitis.1 The absence of pharyngeal inflammation or the presence of either rhinorrhea or laryngitis is much more likely to be associated with viral infection. However, no physical findings clearly separate group A beta-hemolytic streptococci (GABHS) from viral, other bacterial, or noninfectious causes.
Multiple etiologies can cause irritation and inflammation of the pharynx. Causes in children range from viruses (eg, adenoviruses, enteroviruses, Epstein-Barr virus [EBV]), which often require only supportive therapy, to bacterial pathogens (eg, GABHS), which require antibiotic therapy. GABHS pharyngitis is spread via respiratory droplets through close contact.
No pathogen is isolated in nearly 30% of cases, and viruses are isolated in approximately 40% of cases. Other probable copathogens in children include Staphylococcus aureus, Haemophilus influenzae, Branhamella catarrhalis, Bacteroides fragilis, Bacteroides oralis, Bacteroides melaninogenicus, Fusobacterium species, and Peptostreptococcus species. Less common causes include Chlamydia trachomatis and Mycoplasma pneumoniae.
GABHS is the primary organism of concern in most pediatric cases of pharyngitis because appropriate antibiotic therapy is effective and can eliminate complications of rheumatic heart disease. For all cases, including viral etiologies, supportive care is necessary to prevent associated symptoms such as dehydration.
Approximately 10% of children seen by medical care providers each year have pharyngitis, and 25-50% of these children have GABHS. Approximately 20% of asymptomatic children are chronic carriers of GABHS.
The entire range of pharyngitis-causing pathogens is observed throughout the world. Certain pathogens that are virtually nonexistent in the United States cause pharyngitis in other areas. A good example is diphtheria, which has been nearly eradicated in the United States through immunizations. According to the Red Book, from 1990-1995, approximately 48,000 cases of epidemic diphtheria were reported in the former Soviet Union and central Asia.3 Given the high case-fatality rate of 3-23% and the increased mobility of people, the potential for worldwide spread of diphtheria is a cause for concern. Consider rare or unsuspected causative agents in afflicted individuals who have traveled to high-risk areas or for individuals who have emigrated from these regions, especially in nonimmunized patients.
Prevalence is equal among all races.
Peak prevalence of GABHS pharyngitis is in children aged 5-10 years. In children younger than 2 years, most pharyngitis is of viral etiology, although GABHS is responsible in rare instances. Viral pharyngitis occurs in persons of all ages.
Diphtheria
Mononucleosis and Epstein-Barr Virus
Infection
Mycoplasma Infections
Coxsackievirus infection
The following studies are necessary in individuals with suspected pharyngitis:
Penicillin is the typical therapy for group A beta-hemolytic streptococci (GABHS) pharyngitis, in conjunction with prevention of dehydration and supportive care for pain. Improved compliance with regimens has been noted when penicillin treatment is administered 2-3 times daily, as compared with traditional regimens with 4 daily doses. Administer a minimum of 20 mg/kg/d; larger children are generally administered 500 mg divided into 2 daily doses for 10 days.
Several other medications, including some that are more palatable and meet with better compliance (eg, amoxicillin), have been approved to treat GABHS. Treat relapses or failure to improve with an antibiotic active against beta-lactamase–producing organisms (ie, macrolides, cephalosporins, amoxicillin/clavulanate). The hypothesis is that colonizing pharyngeal bacteria that produce penicillinase have inactivated penicillin, resulting in treatment failure.
Recently, corticosteroids (eg, oral dexamethasone) have been suggested as an adjunctive therapy to decrease pain and length of symptoms in adults with pharyngitis. One randomized controlled study in children found that the use of single-dose oral dexamethasone (0.6 mg/kg, not to exceed 10 mg) did not decrease the time to onset of clinically significant pain relief or the time to complete pain relief.6 However, for the subset of children with positive rapid streptococcal test results, improvement in the time to onset of pain relief was statistically significant (but marginally clinically significant).
These agents are used to treat recurrent GABHS pharyngitis.
Often used in place of penicillin, but it has not been demonstrated to be more effective. Amoxicillin binds to PBPs, inhibiting bacterial cell wall growth.
250-500 mg PO tid; not to exceed 3 g/d
25-50 mg/kg/d PO divided q8h for 10 d
>2 years: Recent study showed that 750 mg/d PO for 10 d was as effective as 250 mg PO tid
Reduces efficacy of PO contraceptives; increased serum concentration with coadministration of probenecid
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in documented hypersensitivity to cephalosporin; caution in renal dysfunction (consider dosage modification), consider consultation with a nephrologist; increased risk of maculopapular rash with EBV, acute lymphocytic leukemia, and CMV
Binds to the 50S ribosomal subunit of the bacteria, inhibiting protein synthesis.
500 mg PO on day 1, followed by 250 mg PO on days 2-5
12 mg/kg/d PO for 5 d; not to exceed 500 mg/d
Limited studies have examined possible interactions; possible interaction with drugs that interact with erythromycin (eg, theophylline, digoxin, anticoagulants); do not administer with antacids
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Patients who have an allergic reaction to azithromycin need a longer-than-usual observation period given the medication's long half-life; caution in impaired liver function; possible adverse drug reactions with GI symptoms (eg, diarrhea, abdominal pain, nausea, vomiting)
Has been shown to be effective in more than 90% of cases. Penicillin binds to PBPs, inhibiting bacterial cell wall growth.
1.2 million U IM as a single dose
25,000-50,000 U/kg IM as a single dose; not to exceed 1.2 million U
<27.3 kg: 300,000-600,000 U IM as a single dose
>27.3 kg: 900,000-1,200,000 U IM as a single dose
Increased serum concentration with probenecid
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function; for deep IM administration only; do not administer IV, SQ, or intra-arterially
DOC for patients who can tolerate PO therapy. Inhibits the biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached, and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.
250 mg PO tid/qid for 10 d
<27.3 kg: 125 mg PO tid/qid for 10 d
>27.3 kg: Administer as in adults
Increased serum concentrations with probenecid
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in cephalosporin allergies and renal impairment; administer 1 h ac or 2 h pc
Recommended by the AAP for patients who are allergic to penicillin. Erythromycin binds to the 50S ribosomal subunit of the bacteria, inhibiting protein synthesis.
400-800 mg (as the ethylsuccinate salt) PO qid
40 mg/kg/d PO divided tid/qid for 10 d
Potent inhibitor of CYP450 3A4; coadministration may increase toxicity of CYP450 3A4 substrates (eg, theophylline, digoxin, carbamazepine, cyclosporine); may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin, increases risk of rhabdomyolysis; decreases metabolism of repaglinide, thus increasing serum levels and effects
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in hepatic impairment; commonly causes GI symptoms (eg, abdominal pain, diarrhea, nausea, vomiting)
Can be used for recurrent GABHS pharyngitis or in carrier-state cases. Inhibits bacterial protein synthesis by its action at the bacterial ribosome. The antibiotic binds preferentially to the 50S ribosomal subunit and affects the process of peptide chain initiation. Some prefer this medication when treating disease related to peritonsillar abscesses that have been drained.
150-300 mg PO tid
30 mg/kg/d PO divided tid for 10 d; not to exceed 1.8 g/d
Increased neuromuscular block with coadministration of pancuronium and tubocurarine
Documented hypersensitivity; hepatic impairment prior pseudomembranous colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Renal or hepatic impairment; may cause pseudomembranous colitis; administer cap with full glass of water
Recommended in conjunction with penicillin for recurrent GABHS and for carrier states. Inhibits RNA synthesis in bacteria by binding to beta subunit of DNA-dependent RNA polymerase, which, in turn, blocks RNA transcription.
10 mg/kg/d PO as a single dose; not to exceed 600 mg/d
Used in conjunction with penicillin VK for 10 d, 20 mg/kg/d PO divided qid for the last 4 d
Alternately, 10 mg/kg PO q12h for 4 d in conjunction with benzathine penicillin
Induces microsomal enzymes, which may decrease effects of acetaminophen, PO anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, PO contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid or pyrazinamide may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFT results occur)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hepatic impairment; monitor for any severe flulike symptoms; administer on an empty stomach; may discolor urine, tears, sweat, or other body fluids
Second-generation cephalosporin that maintains gram-positive activity of first-generation cephalosporins; adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis.
Resists degradation by beta-lactamase. Very effective against copathogens. A broad variety of cephalosporins (especially second-generation) have been used; however, their ability to prevent rheumatic heart disease is not known.
The oral susp and tabs are not bioequivalent and require different dosage regimens.
250-500 mg PO bid
Susp: 20 mg/kg/d PO divided bid; not to exceed 500 mg/d
Tab: 125 mg PO bid
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after administration; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patient receiving potent diuretics (eg, loop diuretics); coadministration with aminoglycosides increases nephrotoxic potential
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Administer one-half dose if CrCl is 10-30 mL/min and one-fourth dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy
Third-generation cephalosporin with broad-spectrum gram-negative activity. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
1-2 g/d IM for 10 d
50 mg/kg/d IM for 10 d; not to exceed 1 g/d
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in breastfeeding women and those who are allergic to penicillin; adjust dose in renal impairment
Semisynthetic cephalosporin administered as prodrug. Hydrolyzed by esterases during absorption and distributed in circulating blood as active cefditoren.
Bactericidal activity results from inhibition of cell wall synthesis via affinity for penicillin-binding proteins.
No dose adjustment necessary for mild renal impairment (CrCl 50-80 mgL/min/1.73 m2) or mild-to-moderate hepatic impairment.
Indicated for the treatment of acute exacerbation of pharyngitis/tonsillitis caused by susceptible strains of Streptococcus pyogenes.
200 mg PO bid pc for 10 d
<12 years: Not established
>12 years: Administer as in adults
Severe renal impairment (ie, CrCl <30 mL/min/1.73 m2): Decrease dose to 200 mg PO qd
Absorption reduced with H2-receptor antagonists and magnesium and aluminum hydroxide antacids may reduce absorption; probenecid may increase plasma concentrations
Documented hypersensitivity to drug, penicillin, related compounds, or milk protein sodium caseinate; carnitine deficiency or inborn errors of metabolism that may result in clinically significant carnitine deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May cause diarrhea, nausea, and vaginal moniliasis (yeast infection); pseudomembranous colitis may occur; clinical manifestations of carnitine deficiency may occur with prolonged use; prolonged use may result in emergence and overgrowth of resistant organisms; caution in breastfeeding
These agents may be used adjunctively to antibiotics to improve pain relief onset and are especially useful in patients with positive rapid streptococcal antigen test results.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Possesses many pharmacologic benefits but also significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates and improves pulmonary microcirculation.
Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.
Patients can be switched from an IV to PO regimen in a 1:1 ratio.
For pharyngitis, corticosteroids must be administered in conjunction with antibiotics. Provides symptomatic relief for severe pharyngitis. A one-time IM dose is convenient and avoids compliance issues.
0.75-9 mg/d PO/IM/IV in divided doses q6-12h
0.6 mg/kg PO once; if multiple doses used, not to exceed 10 mg/m2/d divided q6-12h
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Most adverse effects of corticosteroids are dose-dependent or duration-dependent; increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
[Guideline] Michigan Quality Improvement Consortium. Acute pharyngitis in children. Southfield (MI): Michigan Quality Improvement Consortium; 2009 Jan. [Full Text].
Fretzayas A, Moustaki M, Kitsiou S, Nychtari G, Nicolaidou P. The clinical pattern of group C streptococcal pharyngitis in children. J Infect Chemother. Aug 2009;15(4):228-32. [Medline].
American Academy of Pediatrics. Report of the committee on infectious diseases. Pickering LK, Baker CJ, McMillan J, Long S (Editors). Red Book. 27th Edition. Elk Grove Village, Il: American Academy of Pediatrics; 2006:430-439.
el-Daher NT, Hijazi SS, Rawashdeh NM, et al. Immediate vs. delayed treatment of group A beta-hemolytic streptococcal pharyngitis with penicillin V. Pediatr Infect Dis J. Feb 1991;10(2):126-30. [Medline].
Wannamaker LW, Rammelkamp CH Jr, Denny FW, et al. Prophylaxis of acute rheumatic fever by treatment of the preceding streptococcal infection with various amounts of depot penicillin. Am J Med. Jun 1951;10(6):673-95. [Medline].
Bulloch B, Kabani A, Tenenbein M. Oral dexamethasone for the treatment of pain in children with acute pharyngitis: a randomized, double-blind, placebo-controlled trial. Ann Emerg Med. May 2003;41(5):601-8. [Medline].
Chi H, Chiu NC, Li WC, Huang FY. Etiology of acute pharyngitis in children: is antibiotic therapy needed?. J Microbiol Immunol Infect. Mar 2003;36(1):26-30. [Medline].
Denny FW, Wannamaker LW, Brink WR, et al. Landmark article May 13, 1950: Prevention of rheumatic fever. Treatment of the preceding streptococcic infection. JAMA. Jul 26 1985;254(4):534-7. [Medline].
Edress D. Dosing Handbook. 4th ed. Egleston Scottish Rite Children's Healthcare System; 1999-2000.
Feder HM Jr, Gerber MA, Randolph MF, et al. Once-daily therapy for streptococcal pharyngitis with amoxicillin. Pediatrics. Jan 1999;103(1):47-51. [Medline]. [Full Text].
Gerber MA. Diagnosis and treatment of pharyngitis in children. Pediatr Clin North Am. Jun 2005;52(3):729-47, vi. [Medline].
Gerber MA, Markowitz M. Management of streptococcal pharyngitis reconsidered. Pediatr Infect Dis. Sep-Oct 1985;4(5):518-26. [Medline].
Krober MS, Weir MR, Themelis NJ, van Hamont JE. Optimal dosing interval for penicillin treatment of streptococcal pharyngitis. Clin Pediatr (Phila). Nov 1990;29(11):646-8. [Medline].
Marvez-Valls EG, Stuckey A, Ernst AA. A randomized clinical trial of oral versus intramuscular delivery of steroidsin acute exudative pharyngitis. Acad Emerg Med. Jan 2002;9(1):9-14. [Medline].
Peter G, Smith AL. Group A streptococcal infections of the skin and pharynx (second of two parts). N Engl J Med. Aug 18 1977;297(7):365-70. [Medline].
Pichichero ME. Controversies in the treatment of streptococcal pharyngitis. Am Fam Physician. Dec 1990;42(6):1567-76. [Medline].
Roosevelt GE, Kulkarni MS, Shulman ST. Critical evaluation of a CLIA-waived streptococcal antigen detection test inthe emergency department. Ann Emerg Med. Apr 2001;37(4):377-81. [Medline].
Smeesters PR, Campos D, Van Melderen L, et al. Pharyngitis in low-resources settings: a pragmatic clinical approach to reduce unnecessary antibiotic use. Pediatrics. Dec 2006;118(6):e1607-11. [Medline].
Snellman LW, Stang HJ, Stang JM, et al. Duration of positive throat cultures for group A streptococci after initiation of antibiotic therapy. Pediatrics. Jun 1993;91(6):1166-70. [Medline].
Van Cauwenberge PB, Vander Mijnsbrugge A. Pharyngitis: a survey of the microbiologic etiology. Pediatr Infect Dis J. Oct 1991;10(10 Suppl):S39-42. [Medline].
pharyngitis, sore throat, tonsillitis, tonsillopharyngitis, nasopharyngitis, pharyngeal inflammation, group A beta-hemolytic streptococci, GABHS, GABHS pharyngitis, viral pharyngitis, rheumatic fever, rhinorrhea, laryngitis, adenoviruses, enteroviruses, treatment, diagnosis
Harold K Simon, MD, MBA, Professor of Pediatrics and Emergency Medicine, Associate Division Director of Pediatric Emergency Medicine, Director of Research, Division of Pediatric Emergency Medicine, Emory University School of Medicine, Children's Healthcare of Atlanta at Egleston
Harold K Simon, MD, MBA is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American Pediatric Society, and Sigma Xi
Disclosure: Nothing to disclose.
Rosemary Johann-Liang, MD, Medical Officer, Infectious Diseases and Pediatrics, Division of Special Pathogens and Immunological Drug Products, Center for Drug Evaluation and Research, Food and Drug Administration
Rosemary Johann-Liang, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine
Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.
Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; sanofi pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching
Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None
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