Bacterial Pharyngitis Clinical Presentation

Updated: Feb 08, 2019
  • Author: Joseph Adrian L Buensalido, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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The signs and symptoms listed below may be seen with many non-GABHS etiologies. Furthermore, individuals with GABHS pharyngitis may have only a few or mild features listed. Conjunctivitis, cough, hoarseness, coryza, diarrhea, anterior stomatitis, discrete ulcerative lesions, and a viral exanthem are all more consistent with an etiology other than GABHS, particularly viral. Recent studies have also included rhinorrhea and conjunctival infection as viral features. [16] Signs and symptoms include the following:

  • Sore throat, usually with sudden onset
  • Odynophagia
  • Headache
  • Nausea, vomiting, and abdominal pain


Physical examination may reveal the following:

  • Fever
  • Tonsillopharyngeal erythema
  • Exudates (patchy and discrete)
  • Beefy red swollen uvula
  • Lymphadenopathy (tender anterior cervical nodes)
  • Petechiae on the palate
  • Scarlatiniform rash (In susceptible hosts, this usually manifests within the first two days of symptoms and causes a finely papular, blanching, and erythematous rash. The neck is often first affected and then spreads along the trunk and limbs. Resolution, often at 3-4 days, occurs in roughly the same order of appearance and often results in desquamation of the involved areas.)

Predictive models have been developed to help determine the likelihood of GABHS pharyngitis based on the presence of fever, swollen tender anterior cervical lymph nodes, and tonsillar exudates and the absence of cough. Scores have been used to distinguish which patients merit further laboratory evaluation or treatment. The use of such clinical algorithms has been the source of much debate. [1, 17] These score systems were originally developed prior to the availability of RADTs and might be helpful in determining which patients to test for GAS pharyngitis but lack sufficient specificity to decide which patients need antibiotic therapy and might result in unnecessary use of antibiotics. [1]



Viruses cause the vast majority of pharyngitis cases. Common agents include coronavirus, rhinovirus, adenovirus, parainfluenza, influenza, Epstein-Barr virus, cytomegalovirus, and HIV.

GABHS accounts for 15%-30% of pharyngitis cases in children and 5%-10% of cases in adults. [1] Bacteria other than GABHS that may cause pharyngitis are discussed below.

Group C and G streptococci

Like GABHS, these pathogenic bacteria cause beta-hemolysis, form large colonies, and produce an M protein, yet neither is detected with RADTs, as they lack the group A antigen, which is the target of the test.

Pharyngitis caused by either of these non-GABHS streptococci have a clinical presentation similar to that of GABHS pharyngitis and should be considered in patients with worsening symptoms and an initial negative RADT result. They have been reported in epidemics, particularly in semi-closed populations such as military installations or schools [18, 19, 20] and in sporadic pharyngitis in college students. [21]

These bacteria are an uncommon cause of acute pharyngitis in pediatric patients. [22, 23] They have not been associated with the development of acute rheumatic fever. [24] Diagnosis can be achieved with a bacterial throat culture and identification based on Lancefield antigens. [25]

The prevalence of group C Streptococcus infection among primary care patients presenting with sore throat was reported to be 6.1% (95% CI, 3.1%-9.2%). [26]

Arcanobacterium haemolyticum

This gram-positive rod is an uncommon cause of pharyngitis and tonsillitis and accounts for 0.5% and 3% of cases. [27] Clinical manifestations are similar to those of GABHS pharyngitis, although about half of patients with A haemolyticum pharyngitis develop a rash, which typically starts on the extensor surfaces; spares the palms, soles, and head; and moves centrally to involve the trunk with a maculopapular or scarlatiniform appearance.

A haemolyticum exhibits variable susceptibility to penicillin and is identified more easily on human or rabbit blood agar than on sheep agar, the media traditionally used to identify GABHS. It is more common in adolescents and young adults. [28] Erythromycin is the treatment drug of choice. [27]

Neisseria gonorrhoeae

Infection with this pathogen is associated with oral-genital contact and is often asymptomatic. [29] N gonorrhoeae may be identified using chocolate or Thayer-Martin agar. [30] Nucleic acid amplification tests from throat rinses appear to be a promising alternative. [31] Because of increasing rates of fluoroquinolone resistance, ceftriaxone is now the only recommended option for treatment of pharyngeal gonorrhea. [32] Treatment aimed at Chlamydia trachomatis is also recommended, since co-infection is common.

Mycoplasma pneumoniae

This atypical bacterium is increasingly being identified as an etiologic agent of pharyngitis. [33] M pneumoniae pharyngitis may be associated with pulmonary findings. [34]

Yersinia species

Both Yersinia enterocolitica and Yersinia pestis may cause disease. Pharyngeal plague has been linked to the consumption of camel meat. [35]

Chlamydia trachomatis and Chlamydophila pneumoniae

Both of these organisms are rare causes of pharyngitis. [33, 31]

Francisella tularensis (oropharyngeal tularemia)

The causative organism is a gram-negative pleomorphic coccobacillus that can be acquired by ingestion of contaminated water or inadequately cooked game meat. It is an uncommon cause of pharyngitis and tonsillitis in the United States and is usually accompanied by lymphadenitis and severe exudative stomatitis. [36]

Corynebacterium diphtheriae

Toxigenic strains of this gram-positive bacillus are common causes of croup. [37] Young patients with C diphtheriae pharyngitis often exhibit inspiratory stridor, sternal retraction, and a barking cough. In severe cases, a membrane formation may impair breathing. The incidence of C diphtheriae pharyngitis in developed countries is low because of high immunization rates.


This is an anaerobic gram-negative bacillus that can be isolated from the oropharynx of healthy individuals but that has been associated with sore throat. [38] It can also cause life-threatening disease, including Lemierre syndrome or postanginal sepsis (internal jugular vein thrombophlebitis, septic pulmonary emboli, and bacteremia. [39] Some studies also suggest a role for this bacterium in recurrent or persistent sore throat. [40, 41] However, it should always be considered if a patient presents with severe pharyngitis. [42] It is more common in adolescents and young adults.

The prevalence of Fusobacterium necrophorum infection among primary care patients presenting with sore throat was reported to be 19.4% (95% CI, 14.7%-24.1%). [26]



GABHS infection may result in suppurative or nonsuppurative complications.

Local complications: These result from untreated infection that spreads to adjacent sites. Some of the more common of these suppurative infections include retropharyngeal abscess, peritonsillar abscess, sinusitis, cervical lymphadenitis, otitis media, and mastoiditis.

Acute rheumatic fever: This disorder usually occurs 2-4 weeks after an episode of pharyngitis. Administration of proper antibiotics up to 9 days after the onset of pharyngeal symptoms has been shown to prevent this manifestation. [43]  Major manifestations of acute rheumatic fever include carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. Minor criteria include fever, polyarthralgia, elevated leukocyte count, elevated erythrocyte sedimentation rate, and prolonged P-R interval. Current incidence of this complication after endemic infection is unknown but believed to be substantially less than 1%. [44]

Rheumatic heart disease: This is the chronic valvular manifestation of acute rheumatic fever. The mitral valve is the site most often affected, and either regurgitation or stenosis may result. [45]  In individuals with rheumatic heart disease, long-term secondary prophylaxis, often with benzathine penicillin, decreases the risk of subsequent episodes of acute rheumatic fever and further heart damage.

Poststreptococcal glomerulonephritis: This usually occurs 1-3 weeks following GABHS pharyngitis. Poststreptococcal glomerulonephritis, which may also follow a GABHS skin infection, has not been shown to be preventable with proper administration of antibiotics. Patients often present with hematuria, edema, and hypertension.