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Antibiotic failure in the treatment of streptococcal tonsillopharyngitis

Author
Michael E Pichichero, MD
Section Editors
Daniel J Sexton, MD
Sheldon L Kaplan, MD
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

The natural course of group A streptococcal (GAS) tonsillopharyngitis consists of rapid onset of symptoms and signs of infection with spontaneous resolution of symptoms within two to five days. Given the self-limited nature of symptoms of this infection, goals of antimicrobial therapy include not only reduction in duration and severity of symptoms (if antimicrobial therapy is initiated early) but, more importantly, reduction in duration of infectiousness, prevention of suppurative complications (eg, otitis, sinusitis), and prevention of nonsuppurative complications (eg, acute rheumatic fever and possibly acute glomerulonephritis). (See "Complications of streptococcal tonsillopharyngitis".)

GAS is universally sensitive to penicillin and cephalosporins. Macrolide resistance has been reported in more than 25 percent of GAS strains in Europe and Scandinavia and has also been described in the United States [1,2].

Some patients with streptococcal tonsillopharyngitis fail to achieve clinically persistent and/or microbiological cure after antimicrobial therapy. Factors associated with antibiotic failure in the treatment of streptococcal pharyngitis are reviewed here. The approach to treatment of streptococcal tonsillopharyngitis is discussed separately. (See "Treatment and prevention of streptococcal tonsillopharyngitis".)

FACTORS ASSOCIATED WITH ANTIBIOTIC FAILURE

No single antibiotic regimen eliminates group A Streptococcus (GAS) from the pharynx in 100 percent of cases. There are several potential explanations for antibiotic failure; these include epidemiologic, clinical, and microbiologic factors.

Epidemiologic factors — Crowded living conditions facilitate GAS transmission in households, workplaces, schools, and daycare centers. Recurrent infection with the same serotype following initial treatment may be associated with milder symptoms; these individuals are contagious to others in their environment and are themselves susceptible to acute rheumatic fever [3].

              

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Literature review current through: Nov 2016. | This topic last updated: Thu Apr 02 00:00:00 GMT+00:00 2015.
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