Recent studies suggested that interactions between various organisms, including GABHS, other aerobic and anaerobic bacteria, and viruses, may occur during PT. Some of these interactions may be synergistic (i.e., between EBV and anaerobic bacteria), thus enhancing the virulence of some pathogens, whereas others may be antagonistic (i.e., between GABHS and certain “interfering” α-hemolytic streptococci). Furthermore, β-lactamase-producing bacteria (BLPB) can protect themselves as well as other bacteria from β-lactam antibiotics.

Aerobic bacteria

Because of the potential of serious suppurative and nonsuppurative sequelae, GABHS are the best known cause of sore throat. Occasionally non groups B, and large colony C, and G β-hemolytic streptococci are responsible. However, the other groups are generally not associated with acute rheumatic fever.

The clinical presentation of PT is generally identical for all groups and is characterized by exudation, palatal petechiae, follicles, tender cervical adenitis, and scarlet fever rash. What are generally absent are the classical signs of viral infections such as cough, rhinitis, conjunctivitis, and diarrhea.

There is no symptom or single sign that reliably identifies GABHS pharyngitis. Symptoms in children younger than 3 years of age are atypical and include nasal congestion and discharge, low-grade fever, and tender anterior cervical lymph nodes. GABHS should be suspected in the presence of abrupt onset of fever in a child older than 3 years (with or without “sore throat”), higher temperature, ill appearance, headache, neck muscle pain, tenderness, abdominal pain, nausea, or vomiting, flushed cheeks, circumoral pallor, palatal “petechiae” and semicircular red marks, early strawberry tongue and/or scarlatiniform rash, a history of exposure to the organism, winter season, and the presence of a peculiar, sour-sweet, yeasty breath odor.

The isolation rate of GABHS varies with patient age, with the highest prevalence in school years (15%–30% of all PT). The isolation rate of non-GABHS is higher in adults than in children.

There was a marked decrease in the incidence of acute rheumatic fever in the United States over the past 50 years that is correlated with the replacement of rheumatogenic types by nonrheumatogenic types. However, streptococcal tonsillitis is still a potential serious illness because rheumatic fever still occurs, and GABHS is manifesting increased virulence. More cases of sepsis, pneumonia, and toxic shock syndrome due to streptococci have been observed in recent years. Streptococci can be involved in suppurative complications of tonsillitis such as peritonsillar and retropharyngeal abscesses.

Streptococcus pneumoniae can also be involved in PT that can either subside or spread to other sites.

Corynebacterium diphtheriae can cause a “bull neck,” as can Arcanobacterium hemolyticum, and both can cause an early exudative PT with a grayish-green thick membrane that may be difficult to dislodge and often leaves a bleeding surface when torn off. The infection can spread to the throat, palate, and larynx. It is rare in developed countries where children are vaccinated against it. Arcanobacterium hemolyticum produces a lethal systemic exotoxin.

Arcanobacterium hemolyticum incidence of causing PT is 2.5% to 10%, and occurs mostly in 15- to 18-year-old individuals, and about half of the patients have a scarlatiniform rash.

Neisseria gonorrheae is common in homosexual males and can be detected in sexually active adolescents with pharyngitis. The infection is often asymptomatic but can exhibit ulcerative or exudative pharyngitis, may result in bacteremia, and can persist after treatment. Neisseria meningitidis can cause symptomatic or asymptomatic PT that can be a prodrome for septicemia or meningitis.

Nontypeable Haemophilus influenzae and Haemophilus parainfluenzae can be recovered from inflamed tonsils. These organisms can cause invasive disease in infants and elderly persons, as well as acute epiglottitis, otitis media, and sinusitis.

Staphylococcus aureus is often recovered from chronically inflamed tonsils and peritonsillar abscesses. Methicillin-resistant S. aureus (MRSA) was isolated from 16% of recurrently infected tonsils. It can produce the enzyme β-lactamase that may interfere with the eradication of GABHS. High tissue concentration of H. influenzae, S. aureus, and GABHS correlates with recurrent infection and hyperplasia of the tonsils.

Francisella tularensis infection (tularemia) is rare and should be considered in patients unresponsive to penicillin. It can be contracted by ingestion of contaminated water such as in poorly cooked wild animal meat. Clinical presentation of PT includes fever, painful ulcerative-exudative pharyngitis, and cervical lymphadenitis.

Other rare causes of PT are Treponema pallidum, Mycobacterium spp., and Toxoplasma gondii.

Anaerobic bacteria

The anaerobic species that have been implicated in PT are Actinomyces spp., Fusobacterium spp., and pigmented Prevotella and Porphyromonas spp.

The role of anaerobes is supported by their predominance in tonsillar or retropharyngeal abscesses and Vincent’s angina (Fusobacterium spp. and spirochetes). Furthermore, patients with non-GABHS tonsillitis as well as infectious mononucleosis respond to antibiotics directed only against anaerobes (metronidazole), and elevated serum levels of antibodies to Prevotella intermedia and Fusobacterium nucleatum were found in patients with recurrent non-GABHS tonsillitis and peritonsillar cellulitis and abscess.

Fusobacterium necrophorum has been recovered in recent studies from the United Kingdom and Denmark of adolescents and young adults with nonstreptococcal PT. Other studies also suggest a role for F. necrophorum in recurrent or persistent sore throat. It is also the etiology of most cases of Lemierre’s syndrome, which generally occurs in previously healthy adolescents and young adults. The syndrome includes necrotizing tonsillopharyngitis associated with Fusobacterium bacteremia, septic internal jugular vein thrombophlebitis, and metastatic pulmonary infection. Clinical findings include fever (>39°C), rigors, respiratory symptoms, and unilateral neck pain and/or swelling.

Mycoplasma

Mycoplasma pneumoniae and Mycoplasma hominis can cause PT usually as a manifestation of a generalized infection. Mycoplasma accounts for 5–15% of cases of PT, and most cases occur in those older than 6 years.

Chlamydia

Chlamydia pneumoniae may cause PT in young adults, often accompanying pneumonia or bronchitis.

Viruses

Viral PT is generally characterized by the absence of an exudate, the presence of ulcerative lesions, minor nontender adenopathy, enanthems, cough, rhinitis, hoarseness, conjunctivitis, or diarrhea.

The viruses known to cause PT are adenovirus (concomitant conjunctivitis), Coxsackie A virus, influenza and parainfluenza viruses (seasonal with high fever, cough, headache, and myalgias), coronavirus, enteroviruses (posterior pharyngeal vesicles or ulcers, vesicles on palms and soles in summer), Epstein–Barr virus (exudative pharyngitis, liver and spleen enlargement, cervical adenopathy), herpes simplex (or HSV, most caused by HSV-1, anterior oral and lip ulcers, fever), rhinovirus, respiratory syncytial virus (RSV), rubeola (oral erythema and Koplik spots prior to exanthema), and cytomegalovirus (CMV).

Primary human immunodeficiency virus (HIV) infection may cause an acute retroviral syndrome which is similar to infectious mononucleosis. The symptoms usually occur within days to weeks after exposure and infection includes fever, weight loss, rash, lymphadenopathy, and splenomegaly.

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