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Pediatric Pharyngitis Medication

  • Author: Harold K Simon, MD, MBA; Chief Editor: Russell W Steele, MD  more...
 
Updated: Apr 26, 2016
 

Medication Summary

Penicillin is the typical therapy for group A beta-hemolytic streptococci (GABHS) pharyngitis, in conjunction with prevention of dehydration and supportive care for pain. Many pediatricians prefer amoxicillin oral suspension simply because the taste is much better. Several other antibiotics (eg, macrolides, cephalosporins, amoxicillin-clavulanate) have also been approved to treat GABHS infection. Corticosteroids (eg, oral dexamethasone) have been suggested as an adjunctive therapy; they are not routinely recommended but can be considered.

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Antibiotics, Other

Class Summary

Antibiotics are used to treat recurrent GABHS pharyngitis. Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of this clinical setting.

Amoxicillin (Moxatag)

 

Amoxicillin is often used in place of penicillin, but it has not been demonstrated to be more effective. Amoxicillin binds to penicillin-binding proteins (PBPs), inhibiting bacterial cell wall growth.

Azithromycin (Zithromax, Zmax)

 

Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. The drug concentrates in phagocytes and fibroblasts, as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.

Azithromycin is used to treat mild-to-moderate microbial infections. The shorter course and once-daily dosing make it a good alternative for patients who are sensitive to penicillin. Pharyngitis-specific dosing should be used.

Penicillin G benzathine (Bicillin L-A)

 

Penicillin G has been shown to be effective in more than 90% of cases. It binds to PBPs and interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Penicillin G is not to be administered intravenously (IV), intra-arterially (IA), or subcutaneously (SC).

Penicillin VK

 

Penicillin VK is the drug of choice for patients who can tolerate oral therapy. It inhibits the biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached and is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

Erythromycin ethyl succinate (E.E.S, EryPed, Ery-Tab)

 

Erythromycin is recommended by the American Academy of Pediatrics (AAP) for patients who are allergic to penicillin. It binds to the 50S ribosomal subunit of the bacteria, inhibiting protein synthesis. Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes and thus causing RNA-dependent protein synthesis to arrest. It is used for treatment of staphylococcal and streptococcal infections.

Clindamycin (Cleocin)

 

Clindamycin is a lincosamide used for treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci) and can be used for recurrent GABHS pharyngitis or in carrier-state cases. Clindamycin inhibits bacterial protein synthesis by its action at the bacterial ribosome; it 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. The capsule should be taken with a full glass of water.

Rifampin (Rifadin)

 

Rifampin is recommended in conjunction with penicillin for recurrent GABHS infection and for carrier states. The drug inhibits RNA synthesis in bacteria by binding to the beta subunit of DNA-dependent RNA polymerase, which, in turn, blocks RNA transcription; it does not inhibit the mammalian enzyme. It should be taken on an empty stomach.

Cefuroxime (Ceftin, Zinacef)

 

Cefuroxime is a second-generation cephalosporin that maintains the gram-positive activity of first-generation cephalosporins while adding activity against Proteus mirabilis,Haemophilus influenzae,Escherichia coli,Klebsiella pneumoniae, and Moraxella catarrhalis. It resists degradation by beta-lactamase and is very effective against copathogens. A broad variety of cephalosporins (especially second-generation agents) have been used; however, their ability to prevent rheumatic heart disease is not known.

The oral suspension and the tablets are not bioequivalent and require different dosage regimens. The condition of the patient, the severity of infection, and the susceptibility of the microorganism determine the proper dose and route of administration. The drug should be administered with food to minimize adverse gastrointestinal (GI) effects.

Ceftriaxone (Rocephin)

 

Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity. It arrests bacterial growth by binding to 1 or more PBPs.

Cefditoren (Spectracef)

 

Cefditoren is a semisynthetic cephalosporin administered as a prodrug. It is hydrolyzed by esterases during absorption and distributed in circulating blood as active cefditoren. Its bactericidal activity results from inhibition of cell wall synthesis via affinity for PBPs.

Cefditoren is indicated for the treatment of acute exacerbation of pharyngitis or tonsillitis caused by susceptible strains of Streptococcus pyogenes. No dose adjustment necessary for mild renal impairment (creatinine clearance 50-80 mL/min/1.73 m2) or mild-to-moderate hepatic impairment.

Cefixime (Suprax)

 

Cefixime acts by binding to 1 or more of the PBPs. It arrests bacterial cell wall synthesis and inhibits bacterial growth. It should be administered with food to minimize adverse GI effects.

Cefpodoxime proxetil

 

Cefpodoxime is a second-generation cephalosporin that is indicated for the management of infections caused by susceptible mixed aerobic-anaerobic microorganisms. It inhibits bacterial cell wall synthesis by binding to 1 or more of the PBPs. Bacteria eventually lyse because of the ongoing activity of cell-wall autolytic enzymes while cell-wall assembly is arrested.

Cephalexin (Keflex)

 

Cephalexin is a first-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. It is bactericidal and effective against rapidly growing organisms forming cell walls. Resistance develops through alteration of PBPs.

Cephalexin is effective for treating infections caused by streptococci or staphylococci, including penicillinase-producing staphylococci, and it is at least as effective as erythromycin in eradicating GABHS infection. Cephalexin may be used to initiate therapy when streptococcal or staphylococcal infection is suspected. It is used orally when outpatient management is indicated.

Cefadroxil

 

Cefadroxil is a first-generation semisynthetic cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms, including S aureus, S pneumoniae, S pyogenes, Moraxella catarrhalis, E coli, Klebsiella species, and Proteus mirabilis.

Amoxicillin-clavulanate (Augmentin, Amoclan)

 

Amoxicillin-clavulanate is a combination drug that includes an antibiotic and a blocking agent (clavulanic acid). It interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli. These agents may be used adjunctively with antibiotics to hasten the onset of pain relief and are especially useful in patients with positive rapid streptococcal antigen test results.

Dexamethasone (Baycadron)

 

Dexamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reducing capillary permeability. It possesses many pharmacologic benefits but also has significant adverse effects.

Dexamethasone stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines. The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. The drug suppresses lymphocyte proliferation through direct cytolysis, inhibits mitosis, breaks down granulocyte aggregates, and improves pulmonary microcirculation.

Potential adverse effects include hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

Dexamethasone provides symptomatic relief for severe pharyngitis. In this setting, it must be administered in conjunction with antibiotics. Dexamethasone is readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. The drug lacks the salt-retaining property of hydrocortisone. Patients can be switched from an IV regimen to an oral regimen in a 1:1 ratio. A single IM dose is convenient and avoids compliance issues.

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Contributor Information and Disclosures
Author

Harold K Simon, MD, MBA Professor of Pediatrics and Emergency Medicine, Vice Chair Department of Pediatrics, Associate Division Director of Pediatric Emergency Medicine, Director of Research, Divison 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: Academic Pediatric Association, American Pediatric Society, American Academy of Pediatrics, Sigma Xi

Disclosure: Received grant/research funds from Venaxis Pharma for study investigator unrelated to these works; Received consulting fee from Venaxis Pharma for board membership; Received grant/research funds from Baxter Pharma for study investigator unrelated to hesse works.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

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, Southern Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College 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.

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.

Garry Wilkes, MBBS, FACEM Director of Emergency Medicine, Calvary Hospital, Canberra, ACT; Adjunct Associate Professor, Edith Cowan University, Western Australia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

References
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Posterior pharynx with petechiae and exudates in a 12-year-old girl. Both the rapid antigen detection test and throat culture were positive for group A beta-hemolytic streptococci.
Streptococcal pharyngitis , Note the redness and edema of the oropharynx, and petechiae, or small red spots, on the soft palate caused by Strep throat. Strep throat is caused by group A streptococcus bacteria. These bacteria are spread through direct contact with mucus from the nose or throat of persons who are infected, or through contact with infected wounds or sores on the skin.
 
 
 
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