> Table of Contents > Parotitis, Acute and Chronic
Parotitis, Acute and Chronic
Colleen W. Meehan, MD, MPH
Kathleen Ferrer, MD, AAHIVS
image BASICS
  • Parotitis is inflammation of the parotid gland caused by infection (viral or bacterial), noninfectious systemic illnesses, mechanical obstruction, or medications.
  • Parotitis can be unilateral or bilateral, acute or chronic. Unilateral parotitis is usually associated with duct obstruction, whereas bilateral parotitis more commonly indicates a systemic cause.
  • The parotid gland is the largest of the salivary glands, located lateral to the masseter muscle anteriorly and extending posteriorly over the sternocleidomastoid muscle behind the angle of the mandible. It produces exclusively serous secretions, which lack the bacteriostatic properties of mucinous secretions, making the parotid gland more susceptible to infection than other salivary glands.
  • The parotid duct, also called Stensen duct, pierces the buccinator muscle to enter the buccal mucosa just opposite the second maxillary molar.
  • The branches of the 7th cranial nerve or “facial nerve” divide the gland into lobes.
  • The parotid gland contains lymph nodes.
  • Viral parotitis is the most common cause of parotitis in children, though the exact incidence is unknown and has decreased since the advent of the mumps vaccine.
  • Acute bacterial parotitis occurs more frequently in elderly patients, neonates (especially preterm infants), and postoperative patients.
  • Neonatal parotitis and juvenile recurrent parotitis are more common in males than females.
  • Juvenile recurrent parotitis is the second most common inflammatory cause of parotitis in children in the United States; first episode usually occurs between the ages of 3 and 6 years.
  • Chronic parotitis mainly affects adults, more often females. The average age of presentation is between 40 and 60 years.
  • Chronic bilateral parotid enlargement is a common manifestation of HIV infection; for perinatally HIV-infected children, the average age of onset for parotid enlargement is 5 years.
  • Acute viral parotitis: lack of mumps, measles, rubella (MMR) vaccination
  • Acute bacterial parotitis
    • Conditions that predispose to salivary stasis such as dehydration, debilitation, poor oral hygiene, Sjögren syndrome, cystic fibrosis, bulimia/anorexia, sialolithiasis (stones), ductal stenosis, trauma
    • Immunosuppression, HIV, chemotherapy, radiation, malnutrition, alcoholism
  • Neonatal parotitis: prematurity, low birth weight, ductal obstruction, oral trauma, structural abnormalities, immunosuppression
  • Juvenile recurrent parotitis: dental malocclusion, congenital duct malformation, genetic factors, immunologic anomalies
  • Drug-induced parotitis: medications such as anticholinergics, antihistamines, diuretics, tricyclic antidepressants, antipsychotics, antineoplastic agents, and iodine
  • Chronic parotitis: ductal stenosis, HIV, tuberculosis, Sjögren syndrome, and sarcoidosis
  • MMR vaccination with the first dose between 12 and 15 months and second dose between 4 and 6 years of age; of note, mumps vaccination does not guarantee prevention, possibly due to waning immunity in adolescence
  • Maintain adequate hydration and good dental hygiene.
  • Suck on hard or sour candy and use hot compresses with parotid massages to stimulate salivary flow and prevent salivary stasis.
  • Smoking cessation, abstinence from alcohol, and avoidance of chronic purging
  • Acute viral parotitis begins as a systemic infection that localizes to the parotid gland, resulting in inflammation and swelling of the gland.
    • Mumps, or paramyxovirus, has a predilection for the parotid gland and classically has been linked to parotitis.
  • Acute bacterial parotitis results from stasis of salivary flow that allows retrograde introduction of bacterial pathogens into the parotid gland, resulting in localized infection.
  • Acute parotitis pathogens
    • Viral
      • Paramyxovirus (mumps), parainfluenza virus types 1 and 3, influenza A, coxsackie viruses, Epstein-Barr virus (EBV)
      • Cytomegalovirus (CMV) and adenovirus have been seen in patients with HIV.
    • Bacterial
      • Staphylococcus aureus and anaerobes (oral flora) are most commonly seen.
      • Streptococcus pneumoniae, viridans streptococci, Escherichia coli, and Haemophilus influenza (less common)
      • Gram-negative rods such as E. coli, Klebsiella, Enterobacter, and Pseudomonas can be seen in chronically ill or hospitalized patients.
    • Fungal
      • Candida has been isolated in chronically ill or hospitalized patients.
      • Actinomyces can be found in patients with a history of trauma or dental caries.
  • Acute, recurrent parotitis
    • Juvenile recurrent parotitis may be secondary to chronic inflammation; etiology is unknown, but a genetic predisposition may exist.
    • Mechanical: sialolithiasis, ductal stenosis; repeated sialolith formation can lead to ductal wall damage, fibrosis, and stricture formation, which further decreases salivary flow and perpetuates obstruction
    • Pneumoparotitis may occur when air is trapped in the ducts of the parotid gland; may be seen in wind instrument players, glass blowers, scuba divers, and with dental cleaning.
    • Medications: anticholinergics, antihistamines, tricyclic antidepressants, antipsychotics (especially phenylbutazone, thioridazine, clozapine), iodine (especially contrast media), and L-asparaginase (1)[C]
    • Other: diabetes, alcoholism, bulimia, “anesthesia mumps” (possible mechanisms include transient mechanical compression of Stensen duct by airway devices, loss of muscle tone around the Stensen orifice after neuromuscular relaxants, increased salivary secretion, and increased flexion or rotation of the head during general anesthesia)
  • Chronic parotitis may occur due to chronic ductal stenosis but is often due to a chronic infectious or inflammatory condition
    • HIV
    • Tuberculosis, syphilis (rare)
    • Autoimmune: Sjögren syndrome (parotid enlargement, xerostomia, and keratoconjunctivitis)
    • Inflammatory: sarcoidosis
      • Heerfordt syndrome (parotid enlargement, facial palsy, and uveitis) is a rare manifestation of sarcoidosis.
  • Chronic parotitis in HIV-infected patients can be due to the presence of benign lymphoepithelial cysts, follicular hyperplasia of parotid lymph nodes, or diffuse infiltrative lymphocytosis syndrome (DILS), causing infiltration of the parotid gland by CD8 cells.
    • Parotitis may also be secondary to immune reconstitution after initiation of combination antiretroviral therapy in HIV-infected patients.
HIV, Sjögren syndrome, sarcoidosis, sialolithiasis
  • Parotitis is characterized by swelling or enlargement of the parotid gland(s) overlying the masseter muscle; it may obscure the angle of the mandible or cause the ear to protrude upward and outward.
  • Palpation of the parotid gland is best done by using one hand to start at the attachment of the earlobe

    and palpating anteriorly and inferiorly along the mandibular ramus while the other hand simultaneously palpates the Stensen duct orifice.
    • Tender and bilateral suggests viral etiology, whereas tender, erythematous, warm, and unilateral suggests bacterial etiology.
    • Nontender in HIV, tuberculosis, Sjögren sydrome, sarcoidosis
  • Trismus may be noted.
  • Pus from Stensen duct is suggestive of bacterial parotitis or superinfection; opening of duct may appear edematous and erythematous in both bacterial and viral parotitis.
  • In juvenile recurrent parotitis, Stensen duct is often enlarged, dilated, erythematous, and swollen.
  • Halitosis and dental decay are often associated with acute exacerbations.
  • Facial nerve palsy can be seen in severe cases.
  • Lymphoma, neoplasm, lymphangitis, cervical adenitis, otitis externa, dental abscess, odontogenic infections, Ludwig angina, and cellulitis should be considered in the differential.
  • Parotid swelling or enlargement typically obscures the angle of the mandible (unlike cervical adenitis).
  • Involvement of Stensen duct is unique to parotitis.
  • History and physical exam are usually sufficient for diagnosis of parotitis.
  • Performing aerobic culture and Gram stain of purulent drainage from Stensen duct or aerobic and anaerobic culture from needle aspiration of gland or abscess can be helpful to identify causative organism.
    • Anaerobic culture from Stensen duct will likely contain oropharyngeal contamination; hence, it is recommended to perform anaerobic cultures only from needle aspirate fluid.
  • Acute bacterial parotitis often demonstrates an elevated white blood cell count and amylase.
  • For suspected mumps, obtain mumps IgM antibody or mumps reverse transcription-polymerase chain reaction (RT-PCR). A 4-fold increase of mumps IgG antibody indicates infection.
  • Consider sending EBV titers and respiratory virus PCR panel if viral parotitis suspected; CMV titers should be sent in immunocompromised patients.
  • For chronic, recurrent, or nontender parotitis, obtain HIV test, PPD, SS-A SS-B antibodies, rheumatoid factor, and antinuclear antibodies to evaluate for underlying etiology.
  • Consider obtaining ultrasound or CT scan of parotid area to assess for abscess, cystic masses, parotid tumors, ductal stenosis, or sialolithiasis if no response to initial treatment.
  • Consider sialography with chronic parotitis to assess the anatomy and functional integrity of the gland; can be diagnostic and therapeutic.
Diagnostic Procedures/Other
Consider performing a biopsy or fine-needle aspiration of gland if there is suspicion for tuberculosis, Sjögren syndrome, or sarcoidosis.
Test Interpretation
  • Findings characteristic of HIV are described in the “Etiology and Pathophysiology” section.
  • Noncaseating granulomas may be seen in sarcoidosis, and caseating granulomas may be found in tuberculosis.
  • Usually a self-limiting course that requires primarily supportive treatment with rest, adequate hydration, analgesia, and antipyretics
    • Can stimulate glands to produce saliva by sucking on hard candies or glycerin swabs
    • Local heat and gentle massage of gland can provide symptomatic relief.
    • For chronic presentations, encourage good dental hygiene and treat underlying etiology of parotitis (HIV, Sjögren syndrome, etc.).
  • Patients diagnosed with mumps should be isolated with standard and droplet precautions for 5 days after onset of parotid swelling.
  • Viral parotitis: with an uncertain diagnosis or toxic presentation, can empirically initiate antibiotics to cover Staphylococcus aureus, anaerobes (oral flora), and Streptococcus pneumoniae
  • Acute bacterial parotitis
    • Outpatient management: amoxicillin/clavulanate, first-generation cephalosporin, clindamycin
    • Chronically ill or hospitalized: ampicillin/sulbactam or clindamycin and nafcillin; if methicillin resistance is probable, consider vancomycin or linezolid
  • Pilocarpine and cevimeline can stimulate saliva production and inhibit ascending infection as well as provide symptomatic relief for patients with underlying Sjögren syndrome.
  • Consider needle aspiration for bacterial parotitis with abscess formation or clinical deterioration with increasing pain, erythema, and swelling not responding to medication.
  • May perform serial drainage for symptomatic cysts
  • Consider superficial parotidectomy for severe recurrent parotid infections in patients with underlying predisposing etiology (such as Sjögren syndrome).
  • Sialendoscopy with cortisone irrigation is effective and safe for the treatment of juvenile recurrent parotitis; cortisone irrigation alone may be just as effective (2)[A],(3)[C].
  • For sialolithiasis, ductal stenosis, or for patients with >1 recurrence per year, consult otolaryngologist for possible duct ligation, ductoplasty, or parotidectomy.
  • Sclerotherapy with methyl violet or tetracycline has been shown to be effective in the treatment of cysts in HIV parotitis and is also considered definitive treatment for chronic parotitis (4)[C].
Admission is recommended for patients with comorbidities, systemic involvement, and inability to tolerate PO, as well as neonates and patients for whom close outpatient follow-up is not feasible.
Antibiotic therapy initiated at diagnosis combined with adequate hydration should result in improvement within 48 hours. If not, patient should be reevaluated.
  • Ensure adequate fluid intake.
  • Hard or sour candies to promote salivary flow
  • Viral infection in immunocompetent individuals often resolves with excellent prognosis.
  • Parotid cysts found in HIV-infected patients are usually benign lymphoepithelial lesions with infrequent malignant transformation.
  • Increased incidence of malignant lymphoma or lymphoepithelial carcinoma may be seen in patients with Sjögren syndrome.
1. Brooks KG, Thompson DF. A review and assessment of drug-induced parotitis. Ann Pharmacother. 2012;46(12):1688-1699.
2. Ramakrishna J, Strychowsky J, Gupta M, et al. Sialendoscopy for the management of juvenile recurrent parotitis: a systematic review and metaanalysis. Laryngoscope. 2015;125(6):1472-1479.
3. Roby BB, Mattingly J, Jensen EL, et al. Treatment of juvenile recurrent parotitis of childhood: an analysis of effectiveness. JAMA Otolaryngol Head Neck Surg. 2015;141(2):126-129.
4. Berg EE, Moore CE. Office-based sclerotherapy for benign parotid lymphoepithelial cysts in the HIV-positive patient. Laryngoscope. 2009;119(5): 868-870.
Additional Reading
  • Armstrong MA, Turturro MA. Salivary gland emergencies. Emerg Med Clin North Am. 2013;31(2):481-499.
  • Brook I. The bacteriology of salivary gland infections. Oral Maxillofac Surg Clin North Am. 2009;21(3):269-274.
  • Capaccio P, Sigismund PE, Luca N, et al. Modern management of juvenile recurrent parotitis. J Laryngol Otol. 2012;126(12):1254-1260.
  • K11.20 Sialoadenitis, unspecified
  • K11.21 Acute sialoadenitis
  • K11.23 Chronic sialoadenitis
Clinical Pearls
  • History and physical exam are usually sufficient for diagnosis (parotid swelling and tenderness with or without purulent drainage from Stensen duct).
  • In recurrent or chronic cases, consider other underlying etiologies such as HIV.
  • S. aureus and anaerobes (oral flora) are the most common organisms isolated in acute bacterial parotitis.
  • Encouraging good oral hygiene and adequate hydration in chronically ill, debilitated, and hospitalized patients can reduce parotitis occurrence.