Updated: Jan 20, 2009
Viral pharyngitis can be caused by numerous viruses. Acute pharyngitis is an inflammatory syndrome of the pharynx and/or tonsils caused by several different groups of microorganisms. Pharyngitis can be part of a generalized upper respiratory tract infection or a specific infection localized in the pharynx.
Most cases are caused by viruses and occur as part of common colds and influenzal syndromes. For information on bacterial pharyngitis, see the eMedicine article Pharyngitis, Bacterial in the Infectious Diseases volume.
Several viruses can cause viral pharyngitis.
Rhinovirus
More than 100 different serotypes of rhinovirus cause approximately 20% of cases of pharyngitis and 30-50% of common colds. These viruses enter the body through the ciliated epithelium that lines the nose, causing edema and hyperemia of the nasal mucous membranes. This condition leads to increased secretory activity of the mucous glands; swelling of the mucous membranes of the nasal cavity, eustachian tubes, and pharynx; and narrowing of nasal passages, causing obstructive symptoms. Bradykinin and lysyl-bradykinin are generated in the nasal passages of patients with rhinovirus colds, and these mediators stimulate pain nerve endings. The virus does not invade the pharyngeal mucosa. Transmission occurs by large particle aerosols or fomites.
Adenovirus
In children, adenovirus causes uncomplicated pharyngitis (most commonly caused by adenovirus types 1-3 and 5) or pharyngoconjunctival fever. The latter is characterized by fever, sore throat, and conjunctivitis. Unlike rhinovirus infections, adenovirus directly invades the pharyngeal mucosa, as shown by the viral cytopathic effect.
Epstein-Barr virus
Epstein-Barr virus (EBV) is the causal agent of infectious mononucleosis. EBV usually spreads from adults to infants. Among young adults, EBV spreads through saliva and, rarely, through blood transfusion. In addition to edema and hyperemia of the tonsils and pharyngeal mucosa, an inflammatory exudate and nasopharyngeal lymphoid hyperplasia also develop. Pharyngitis or tonsillitis is present in about 82% of patients with infectious mononucleosis.
Herpes simplex virus
Herpes simplex virus (HSV) types 1 and 2 cause gingivitis, stomatitis, and pharyngitis. Acute herpetic pharyngitis is the most common manifestation of the first episode of HSV-1 infection. After HSV enters the mucosal surface, it initiates replication and infects either sensory or autonomic nerve endings. The neurocapsid of the virus is intra-axonally transported to the nerve cell bodies in the ganglia and contiguous nerve tissue. The virus then spreads to other mucosal surfaces through centrifugal migration of infectious virions via peripheral autonomic or sensory nerves. This mode of spread explains the high frequency of new lesions distant from the initial crop of vesicles characteristic of oral-labial HSV infection.
Influenza virus
Pharyngitis and sore throat develop in about 50% of the patients with influenza A and in a lesser proportion of patients with influenza B. Severe pharyngitis is particularly common in patients with type A. The influenza virus invades the respiratory epithelium, causing necrosis, which predisposes the patient to secondary bacterial infection. Transmission of influenza occurs by aerosolized droplets.
Parainfluenza virus
Pharyngitis caused by parainfluenza virus types 1-4 usually manifests as the common cold syndrome. Parainfluenza virus type 1 infection occurs in epidemics, mainly in late fall or winter, while parainfluenza virus type 2 infection occurs sporadically. Parainfluenza virus type 3 infection occurs either epidemically or sporadically.
Coronavirus
Pharyngitis caused by coronavirus usually manifests as the common cold. As in rhinovirus colds, viral mucosal invasion of the respiratory tract does not occur.
Enterovirus
The major groups of enteroviruses that can cause pharyngitis are coxsackievirus and echovirus. Although enteroviruses are primarily transmitted by the fecal-oral route, airborne transmission is important for certain serotypes. Enteroviral lesions in the oropharyngeal mucosa are usually a result of secondary infection of endothelial cells of small mucosal vessels, which occurs during viremia following enteroviral infection in the GI tract.
Respiratory syncytial virus
Transmission of respiratory syncytial virus (RSV) occurs by fomites or large-particle aerosols produced by coughing or sneezing. The pathogenesis of RSV infection remains unclear, although a number of theories exist. Immunologic mechanisms may contribute to the pathogenesis of the severe disease in infants and elderly patients.
Cytomegalovirus
Acute acquired cytomegalovirus (CMV) infection is transmitted by sexual contact, in breast milk, via respiratory droplets among nursery or day care attendants, and by blood transfusion. Infection in the immunocompetent host rarely results in clinically apparent disease. Infrequently, immunocompetent hosts exhibit a mononucleosislike syndrome with mild pharyngitis.
Human immunodeficiency virus
Pharyngitis develops in patients infected with human immunodeficiency virus (HIV) as part of the acute retroviral syndrome, a mononucleosislike syndrome that is the initial manifestation of HIV infection in one half to two thirds of recently infected individuals.
Each year, pharyngitis is responsible for more than 40 million visits to health care providers. Most children and adults experience 3-5 viral upper respiratory tract infections (including pharyngitis) per year.
Worldwide, acute infections of the respiratory tract are one of the main causes of disease, and most of these are due to viruses.
Worldwide, viral pharyngitis is one of the most common causes of absence from school or work. The National Ambulatory Medical Care Survey showed that upper respiratory tract infections, including acute pharyngitis, accounted for 200 annual visits to a physician per 1000 population between 1980-1996. The vast majority of upper respiratory tract infections are due to viruses.
Viral pharyngitis affects all races and ethnic groups equally.
Viral pharyngitis affects both sexes equally.
Viral pharyngitis affects both children and adults, but it is more common in children. For more information on pediatric pharyngitis, see the eMedicine article Pharyngitis in the Pediatrics: General Medicine volume.
Sore throat is the chief symptom in patients with viral pharyngitis. Patients may have additional symptoms that vary based on the causal pathogen. These symptoms are generally not useful in discriminating between the causes of viral pharyngitis because the symptoms produced by the numerous viruses that cause pharyngitis are so similar and commonly overlap each other.
Edema and erythema of the pharynx are typical in viral pharyngitis. The degree of erythema does not correlate with the degree of soreness. Exudate can be present but is generally less effusive than in bacterial pharyngitis.
Streptococcal pharyngitis
Gonococcal pharyngitis
Other bacterial pharyngitis
Peritonsillar abscess
Diphtheria
Pharyngeal candidiasis
Noninfectious pharyngitis (eg, allergies; environmental factors; psychosomatic sore throat; sore throat caused by excessive shouting, cheering, or singing; dryness of the throat caused by nasal blockade, obstructive sleep apnea, palatal dysfunction, or mouth breathing)
Treatment strategies for patients with acute pharyngitis are based on epidemiologic factors, signs and symptoms, and results of laboratory tests.1 Rest, oral fluids, and salt-water gargling (for soothing effect) are the main supportive measures in patients with viral pharyngitis.2
Analgesics and antipyretics may be used for relief of pain or pyrexia. Acetaminophen is the drug of choice. Traditionally, aspirin has been used, but it may increase viral shedding. Aspirin should not be used in children or adolescents, especially with influenza, because of its association with Reye syndrome. One study proved that ibuprofen was superior to acetaminophen for symptomatic relief in children aged 6-12 years. A double-blind randomized study involving adult patients from 27 study centers in Latin America found that 5 days of treatment with celecoxib 200 mg once daily is as effective as diclofenac 75 mg twice daily in the symptomatic treatment of viral pharyngitis.3
Anesthetic gargles and lozenges, such as benzocaine, may be used for symptomatic relief. Hospitalization for intravenous hydration may be necessary when odynophagia is intense.
Antibiotics do not hasten recovery or reduce the frequency of bacterial complications. The risks of prescribing antibiotics in patients with viral pharyngitis include the common side effects of antibiotics (diarrhea, rashes, candidiasis, unplanned pregnancy secondary to oral-contraceptive failure) and the rare occurrence of anaphylaxis.4
Specific treatment of viral infections is available for only a few viruses.
Drinking large amounts of fluid is recommended. No specific dietary restrictions are needed. Soft, cold foods (eg, ice cream, popsicles) are more easily tolerated.
No restriction in activity is required.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
These agents are often helpful in relieving the pain and fever associated with pharyngitis.
Relieves pain by elevation of the pain threshold. Reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.
325-650 mg PO q4-6h prn; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: Administer as in adults
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in persons with chronic alcoholism following various dose levels; contained in many OTC products, and combined use with these products may result in cumulative doses exceeding recommended maximum dose
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d
<6 months: Not established
6 months to 12 years: 5-10 mg/kg/dose PO q4-6h prn; not to exceed 40 mg/kg/d
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase risk of methotrexate toxicity (animal studies only); phenytoin levels may be increased when administered concurrently
Documented hypersensitivity to ibuprofen or other NSAIDs
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Risk of GI ulceration, bleeding, and perforation, particularly in patients with active peptic ulcer disease or with a history of peptic ulcer disease; caution in CHF, hypertension, and decreased renal function (maintenance of renal perfusion highly dependent on renal prostaglandins) and hepatic function (severe hepatic reactions including jaundice and cases of fatal hepatitis have been reported); caution in anticoagulation abnormalities or during anticoagulant therapy (inhibits platelet aggregation); if signs or symptoms of meningitis develop, the possibility of aseptic meningitis related to ibuprofen should be considered; if blurred and/or diminished vision, scotomata, and/or changes in color vision develop, ibuprofen should be discontinued, and visual field and color vision testing should be performed; not recommended in breastfeeding mothers
These agents soothe irritated or inflamed mucous membranes associated with sore throat.
Lozenges or gargle reduces pain associated with pharyngitis. Inhibits neuronal membrane depolarization, blocking nerve impulses.
Dissolve 1 lozenge (10 mg) in mouth q2h prn
<6 years: Not established
>6 years: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Reevaluate the patient if sore throat is severe, persists for more than 2 d, or is accompanied or followed by fever, headache, rash, nausea, or vomiting
These agents are used specifically to treat viral infections. They are available for only a few viruses.
Active against influenza A virus. Has little or no activity against influenza B virus isolates. Mechanism of antiviral action is unclear. Prevents release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. In certain cases, known to prevent virus assembly during virus replication. Treatment begun within 48 h of the onset of symptoms decreases the duration of fever and other symptoms.
200 mg/d PO qd or divided bid; split dosage schedule may reduce adverse CNS effects
>65 years: 100 mg/d PO qd or divided bid
Hemodialysis: 200 mg PO qwk
<1 year: Not recommended
1-9 years: 4.4-8.8 mg/kg/d PO qd or divided bid; not to exceed 150 mg/d
9-12 years: 100 mg PO bid
>12 years: Administer as in adults
Agents with anticholinergic activity potentiate anticholinergic adverse effects; concurrent administration of triamterene/ hydrochlorothiazide may increase plasma concentrations; coadministration of thioridazine has been reported to worsen tremor in elderly patients with Parkinson disease; however, it is not known if other phenothiazines produce similar response; trimethoprim/ sulfamethoxazole may impair renal clearance, resulting in higher plasma concentrations; coadministration of quinine or quinidine decreases renal clearance
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in liver disease, uncontrolled psychosis, eczematoid dermatitis, seizures, and those receiving CNS stimulant drugs; reduce dose in renal dysfunction; do not discontinue this medication abruptly
Inhibits viral replication of influenza A virus H1N1, H2N2, and H3N2 with little or no activity against influenza B virus. Prevents penetration of the virus into the host by inhibiting uncoating of influenza A. Does not appear to interfere with the immunogenicity of inactivated influenza A vaccine. Can be used together during an outbreak.
100 mg PO bid
CrCl <10 mL/min, severe hepatic dysfunction, and elderly nursing home patients: 100 mg PO qd
<10 years: Not recommended
>10 years: Administer as in adults
Acetaminophen and aspirin reduce levels when taken concurrently; cimetidine increases plasma levels when taken concomitantly
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal or hepatic impairment; should be discontinued if seizures develop
Inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, decreases release of viruses from infected cells and thus viral spread. Effective to treat influenza A or B. Start within 40 h of symptom onset. Available as capsules and an oral suspension.
Acute illness: 75 mg PO bid for 5 d
Prophylaxis: 75 mg PO qd for 10 d
Acute illness:
<1 year: Not indicated
>1 year:
<15 kg: 30 mg PO bid for 5 d
>15-23 kg: 45 mg PO bid for 5 d
>23-40 kg: 60 mg PO bid for 5 d
>40 kg: Administer as in adults
Prophylaxis:
<1 year: Not established
>1 year:
<15 kg: 30 mg PO qd for 10 d
>15-23 kg: 45 mg PO qd for 10 d
24-40 kg: 60 mg PO qd for 10 d
>40 kg: Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal impairment, chronic cardiac or respiratory disease, and breastfeeding; do not use in children <1 y (preclinical trials have demonstrated death in young animals, possibly related to immature blood-brain barriers); postmarketing reports (mostly from Japan) of self-injury and delirium in patients with influenza (reports primarily among children), unknown if oseltamivir directly contributes to this behavior (monitor for abnormal behavior throughout treatment period)
Synthetic purine nucleoside analogue with in vitro and in vivo inhibitory activity against HSV-1, HSV-2, and VSV. Inhibitory activity is highly selective because of its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV.
Acute herpetic pharyngitis or gingivostomatitis: 200 mg PO 5 times/d or 400 mg PO tid for 10-14 d
<2 years: Not recommended
>2 years: 20 mg/kg/dose PO qid for 10-14 d; not to exceed 800 mg/d
Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity; decreases the renal clearance of methotrexate with potential toxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure (adjust dose) or when using nephrotoxic drugs; caution in breastfeeding mothers
Prodrug rapidly converted to the active drug acyclovir. More expensive but has a more convenient dosing regimen than acyclovir.
500-1000 mg PO bid
Not established
Probenecid, zidovudine, or cimetidine coadministration prolongs half-life and increases CNS toxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure and coadministration of nephrotoxic drugs; associated with onset of hemolytic uremic syndrome
Prodrug that when biotransformed into active metabolite, penciclovir, may inhibit viral DNA synthesis/replication.
250-500 mg PO tid
Not recommended
Coadministration of probenecid or cimetidine may increase toxicity; coadministration increases bioavailability of digoxin
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure or coadministration of nephrotoxic drugs
Inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. Effective against both influenza A and B. To be inhaled through Diskhaler oral inhalation device. Circular foil discs containing 5-mg blisters of drug are inserted into supplied inhalation device.
Treatment: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO q12h for 5 d; initiate within 2 d of symptom onset
Prophylaxis: 10 mg (2 inhalations, 5 mg/inhalation) inhaled PO qd for 10 d; initiate within 36 h of exposure
Treatment:
<7 years: Not established
>7 years: Administer as in adults
Prophylaxis:
<5 years: Not established
>5 years: Administer as in adults
None reported
Documented hypersensitivity, obstructive airway disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor respiratory status; may cause bronchospasm; caution in breastfeeding
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Cunha BA. Group A streptococcal pharyngitis versus colonization. Intern Med. 1994;15:18-19.
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viral pharyngitis, sore throat, acute pharyngitis, rhinoviral pharyngitis, adenoviral pharyngitis, EBV pharyngitis, HSV pharyngitis, influenzal pharyngitis, parainfluenzal pharyngitis, coronaviral pharyngitis, enteroviral pharyngitis, echoviral pharyngitis, RSV pharyngitis, CMV pharyngitis, cytomegaloviral pharyngitis, common cold, flu, influenza, pharynx, tonsils, upper respiratory tract infection, URTI, rhinovirus, adenovirus, Epstein-Barr virus, EBV, herpes simplex virus, HSV, parainfluenza virus, coronavirus, enterovirus, respiratory syncytial virus, RSV, cytomegalovirus, CMV, human immunodeficiency virus, HIV, coxsackievirus, echovirus, acute retroviral syndrome, infectious mononucleosis, IM, group A beta hemolytic streptococcus, GABHS
KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant Professor of Public Health, University of Texas School of Public Health
KoKo Aung, MD, MPH, FACP is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Ambrish Ojha, MD, Staff Physician, Department of Internal Medicine, Texas Tech University Health Sciences Center
Ambrish Ojha, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.
Carson Lo, MD, Staff Physician, Department of Medicine, Memorial Hermann Southwest Hospital
Carson Lo, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Texas Medical Association
Disclosure: Nothing to disclose.
Gregory William Rutecki, MD, Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University
Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
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