See related editorial, "Acute Pharyngitis: The Case for Empiric Antimicrobial Therapy"

Most patients who seek medical attention for sore throat are concerned about streptococcal tonsillopharyngitis, but fewer than 10% of adults and 30% of children actually have a streptococcal infection. Group A β-hemolytic streptococci (GAS) are most often responsible for bacterial tonsillopharyngitis, although Neisseria gonorrhea, Arcanobacterium haemolyticum (formerly Corynebacterium haemolyticum), Chlamydia pneumoniae (TWAR agent), and Mycoplasma pneumoniae have also been suggested as possible, infrequent, sporadic pathogens. Viruses or idiopathic causes account for the remainder of sore throat complaints. Reliance on clinical impression to diagnose GAS tonsillopharyngitis is problematic; an overestimation of 80% to 95% by experienced clinicians typically occurs for adult patients. Overtreatment promotes bacterial resistance, disturbs natural microbial ecology, and may produce unnecessary side effects. Existing data suggest that rapid GAS antigen testing as an aid to clinical diagnosis can be very useful. When used appropriately, it is sensitive (79% to 88%) in detecting GAS-infected patients and is specific (90% to 96%) and cost-effective. Penicillin has been the treatment of choice for GAS tonsillopharyngitis since the 1950s; 10 days of treatment are necessary for bacterial eradication. A single IM injection of benzathine penicillin is effective and obviates compliance issues. Until the early 1970s, the bacteriologic failure rate for the treatment of GAS tonsillopharyngitis ranged from 2% to 10% and was attributed to chronic GAS carriers. Since the late 1970s, the penicillin failure rate has frequently exceeded 20% in published reports. Explanations for recurrent GAS tonsillopharyngitis include poor patient compliance; reacquisition from a family member or peer, copathogenic colonization by Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis, anaerobes that inactivate penicillin with β-lactamase, or all these organisms; suppression of natural immune response by too-early administration of antibiotics; GAS tolerance to penicillin; antibiotic eradication of normal pharyngeal flora that normally act as natural host defenses; and establishment of a true carrier state. When therapy fails, milder symptoms may occur during the relapse. Several antimicrobials have demonstrated superior efficacy compared with penicillin in eradicating GAS and are administered less frequently to enhance patient compliance. In previously untreated GAS throat infections, cephalosporins produce a 5% to 22% higher bacteriologic cure rate; after a penicillin treatment failure, these differences are greater. Amoxicillin/clavulanate and the extended-spectrum macrolides clarithromycin and azithromycin may also produce enhanced bacteriologic eradication in comparison to penicillin. Future research is needed in the development of more sensitive rapid-detection assays for GAS and other possible pathogens in tonsillopharyngitis and of shorter-course regimens of therapy and in determining the necessity and benefit of treatment of non-GAS tonsillopharyngeal isolates.

[Pichichero ME: Group A streptococcal tonsillopharyngitis: Cost-effective diagnosis and treatment. Ann Emerg Med March 1995;25:390-403.]