Version May 2024
INTRODUCTION — Acute infection of the parotid gland can be caused by a variety of bacteria and viruses. Acute bacterial suppurative parotitis is caused most commonly by Staphylococcus aureus and mixed oral aerobes and/or anaerobes in the setting of debilitation, dehydration, and poor oral hygiene, particularly among older postoperative patients.
The pathogenesis, epidemiology, microbiology, clinical manifestations, diagnosis, differential diagnosis, and treatment of acute bacterial suppurative parotitis will be reviewed here. Deep neck space infections, salivary duct stones, and salivary gland swelling are discussed separately. (See "Deep neck space infections in adults" and "Salivary gland stones" and "Salivary gland swelling: Evaluation and diagnostic approach".)
ANATOMY AND PATHOGENESIS — The parotid glands are located on the sides of the face anterior to the external auditory canal, superior to the angle of the mandible, and inferior to the zygomatic arch. Most of the parotid gland is superficial to the masseter muscle. The gland comprises a superficial lobe and a deep lobe separated by the facial nerve. It consists of 20 to 30 intraparotid and periparotid lymph nodes with lymphatic drainage from the ipsilateral side of the face and forehead, including the auricular region and the external auditory canal [1,2]. Stensen's duct arises from the anterior border of the parotid gland, is 4 to 7 cm long, and narrows to 1.2 mm at the isthmus; the os is 0.5 mm and is opposite the upper second molar (figure 1).
Acute bacterial suppurative parotitis may occur when salivary stasis permits retrograde seeding of the Stensen's duct by mixed oral flora [3]. Ductal obstruction by calculi or tumor may predispose to suppuration. Abscess formation may arise by contiguous infection or hematogenous seeding to the intraparotid or periparotid lymph nodes [1].
EPIDEMIOLOGY AND RISK FACTORS — Acute suppurative parotitis occurs primarily in infants under the age of one or in hospitalized older adults who are dehydrated or intubated during the postoperative period [3-6]. With improved surgical care, oral hygiene, fluid and electrolyte balance, and advent of antibiotics, this condition is now relatively uncommon although the precise incidence is unknown. Older data estimated the incidence to be 0.01 to 0.02 percent among hospitalized older adults and 0.002 to 0.04 percent among postsurgical patients [7,8]. Neonatal suppurative parotitis is uncommon [9] and has an estimated prevalence of 3.8 per 10,000 hospital admissions [10].
Factors that diminish or interrupt the flow of saliva through Stensen’s duct predispose to the development of acute bacterial suppurative parotitis; these include recent intensive teeth cleaning, use of anticholinergic drugs and other drugs that reduce salivary flow, malnutrition, salivary calculi with obstruction, and neoplasm of the oral cavity [3]. Infection of embryogenic cysts, such as the first branchial cleft, may result in frequent recurrent suppurative parotitis [11].
MICROBIOLOGY — The microbiology of acute suppurative parotitis is quite variable and is often polymicrobial. S. aureus is by far the most frequently isolated pathogen, but anaerobes are also common [3,12]. Haemophilus influenzae may play a role in community-acquired infections, while other gram-negative aerobes (eg, Enterobacterales) are often seen in hospitalized patients [5,13]. Klebsiella spp are particularly prevalent among patients with diabetes mellitus from Southeast Asia [14,15]. (See "Clinical features, diagnosis, and treatment of Klebsiella pneumoniae infection".)
The polymicrobial nature of parotid space infections was illustrated in a study of 32 aspirates from patients with acute suppurative parotitis [16]. Aerobic bacteria were isolated in 34 percent, anaerobic bacteria in 41 percent, and mixed aerobic and anaerobic bacteria in 25 percent. S. aureus was the predominant aerobe (in 10 patients), followed by viridans streptococci and H. influenzae (in four patients each). Pigmented Prevotella and Porphyromonas spp, Fusobacterium spp, and Peptostreptococcus spp were the predominant anaerobes. Although rare, risk of Enterobacterales and Pseudomonas aeruginosa is higher in immunocompromised patients and hospital-acquired infections.
Rare causes of suppurative parotitis include Streptococcus pneumoniae, Streptococcus pyogenes, Moraxella catarrhalis, Mycobacterium tuberculosis, nontuberculous mycobacteria, and Actinomyces spp [17,18].
CLINICAL MANIFESTATIONS
Presentation — Suppurative parotitis is characterized by the sudden onset of unilateral firm, erythematous swelling in the preauricular area over the parotid gland. Occasionally, the swelling can extend to the angle of the mandible. This is associated with exquisite local pain and tenderness, and patients may complain of trismus and dysphagia. High fevers, chills, and systemic toxicity may also be present. A subacute onset may suggest the progression to a parotid abscess [19].
However, the clinical presentation can be varied with more subtle findings. In one case series of 17 patients, only 30 percent of patients presented with erythema and only 31 percent had fever [12].
On examination, the area of swelling is typically tender to palpation and often erythematous. However, fluctuance is generally not appreciated because of the dense parotid fascia that overlies the gland. Purulent material may be expressed from the orifice of the Stensen's duct in over one-half of the cases (picture 1). There may also be trismus, clinical evidence of dehydration, or signs of poor oral hygiene.
Leukocytosis and an elevated C-reactive protein are common. An elevated serum amylase level (in the absence of pancreatitis) can be seen in some patients [12], although it is usually normal [20]. Imaging findings are discussed elsewhere. (See 'Imaging' below.)
Complications — Since the parotid space abuts the parapharyngeal space, suppurative parotitis can lead to parapharyngeal space infection and massive swelling of the neck (figure 2). This may lead to respiratory obstruction, septic jugular thrombophlebitis (Lemierre syndrome), bacteremia, and osteomyelitis of the adjacent facial bones [4,21]. Odontogenic source of infection predisposes to complications such as a parotid abscess and osteomyelitis of the mandible [19]. More rare complications include facial nerve palsy [1] and fistulas with the skin [22]. (See "Deep neck space infections in adults", section on 'Parapharyngeal and retropharyngeal space infections' and "Lemierre syndrome: Septic thrombophlebitis of the internal jugular vein", section on 'Clinical manifestations'.)
In rare instances, recurrent infection of the parotid gland may occur, particularly in patients with comorbid conditions, such as diabetes mellitus or in patients with infections of embryogenic cysts.
DIAGNOSIS
Approach to diagnosis — Diagnosis of suppurative parotitis consists of characteristic clinical findings (acute parotid swelling with purulent drainage from Stensen’s duct) with confirmation by imaging (typically ultrasound). (See 'Imaging' below.)
In most cases, the probable diagnosis is evident based on clinical presentation. Suppurative parotitis should be suspected in patients with sudden onset of unilateral erythematous swelling of the parotid gland. Lack of systemic symptoms (eg, fever) or drainage within the oral cavity does not exclude suppurative parotitis. Subacute progression of symptoms suggests the development of a parotid abscess or extension of the infection into deeper tissues (eg, osteomyelitis) [19].
Physical examination should focus on palpating the area of swelling to determine whether it is superficial or involves the parotid gland. Oral examination is necessary to evaluate for any purulent discharge from the opening of the Stensen’s duct (picture 1). Drainage can be expressed by gentle massage of the parotid gland in a posterior to anterior direction (movie 1). When purulent drainage is present, it should be collected and sent to microbiology for Gram stain and culture (see 'Evaluation of microbiology' below). Fluctuance over the parotid gland suggests parotid abscess [19]. Firmness that is nontender on palpation is suggestive of malignancy rather than infection. In the setting of an abscess or suspected malignancy, ultrasound-guided fine needle aspiration should be obtained and sent to microbiology and cytology.
Since suppurative parotitis can lead to serious complications, the physical examination should also include a cranial nerve exam to evaluate for facial nerve palsy, neck exam to evaluate for neck swelling that could suggest parapharyngeal abscess and Lemierre syndrome, and a skin exam to evaluate for parotid gland fistulas (see 'Complications' above). Examination of cervical lymph nodes, ears, and teeth can be helpful in ruling out other causes of facial swelling. (See 'Swelling outside of the parotid gland' below.)
Although some laboratory features are suggestive of suppurative parotitis (eg, elevated C-reactive protein, elevated amylase), they are nondiagnostic and not necessary for evaluation.
Imaging is necessary to confirm the diagnosis, evaluate for complications, and to elucidate any predisposing factors underlying the infection (eg, sialolithiasis). (See 'Imaging' below.)
In rare circumstances, if no clear diagnosis is found on imaging and patient does not respond to empiric antibiotic therapy, surgical exploration is warranted to help with diagnosis and therapy. (See 'Managing poor clinical response or recurrence' below.)
Imaging — Imaging studies confirm the diagnosis and are useful to assess for stones, duct obstruction, solid tumors, and complications (eg, abscess, osteomyelitis). The most common imaging options include ultrasound, computed tomography (CT), and magnetic resonance sialography [17,23].
Initial imaging studies — All patients with suspected diagnosis of suppurative or obstructive parotitis should have an imaging study to confirm the diagnosis and evaluate for the presence of abscess, ductal stones, or tumor mass. Ultrasound is the preferred initial imaging study because it is easily performed, inexpensive, and readily available.
Ultrasound is particularly adept at detecting nodules within the parotid parenchyma and can detect 90 percent of stones 2 mm or larger [24]. In early stages of suppurative parotitis, a diffusely enlarged hypoechoic gland is seen with or without ductal dilatation. In later stages, an abscess may develop revealing a hypoechoic focus surrounded by an irregular echogenic rim [8].
Further evaluation for diagnostic uncertainty or complications — Subsequent choice of imaging depends on the particular concern.
●If an abscess or extraglandular extension is suspected, further evaluation by CT imaging is indicated. CT with contrast is most sensitive in determining the depth and extent of an abscess and in detecting involvement of surrounding structures such as rupture into deep neck spaces. It is the most sensitive tool for differentiating suppurative parotitis (diffuse nonhomogeneous pattern of contrast enhancement) from frank abscess (focal area of fluid attenuation surrounded by rim enhancement) [25].
●In patients with recurrent parotitis or atypical findings on examination in which sialolithiasis and/or malignancy is suspected, magnetic resonance imaging (MRI) and MR sialography is indicated. T1-weighted imaging allows better tissue contrast within the parotid gland while diffusion-weighted MRI helps differentiate sialadenitis from abscess (apparent diffusion coefficient values are typically increased in sialadenitis and decreased in abscess) [24]. MR sialography is noninvasive and does not require intraductal injection of contrast material. It provides the best detail of ductal abnormalities within the parotid gland and is indicated to detect ductal stones, strictures, or obstruction [26]. It has replaced conventional radiograph sialography, which requires intraductal injection of contrast material and is inferior in diagnostic value [17].
●In patients with a suspected fistula, fistulography can help evaluate the extent and course of the fistula into periglandular soft tissues. (See "Salivary gland swelling: Evaluation and diagnostic approach" and "Salivary gland stones".)
●Sialendoscopy is a relatively new and minimally invasive technique for the diagnosis of salivary diseases [27]. This procedure allows for observation of the anatomical course of salivary ducts for evaluation of possible pathologies and enables therapeutic maneuvers such as stone extraction, ductal irrigation or installation of anti-inflammatory medications [28].
Evaluation of microbiology — Purulent fluid should be sent for gram stain and culture. Gram stain is particularly helpful in detecting staphylococci. Specimens should be cultured for both aerobes and anaerobes, as well as fungi and mycobacteria. The primary utility of the culture data is to obtain susceptibility testing of a dominant organism to ensure adequate antibacterial therapy.
Specimens should be collected in the following situations:
●If intraoral drainage is present on exam or can be elicited from the mouth with massage, a swab of fluid should be collected and Gram stain and culture should be sent. However, culture obtained intraorally should be interpreted with caution since the results may represent contamination by the oral flora.
●If a parotid abscess is present, we suggest ultrasound-guided needle aspiration of the abscess by an extraoral route to obtain specimens for microbiologic evaluation prior to empirical antimicrobial therapy [29]. If malignancy is suspected, cytology should be sent on the collected fluid as well.
DIFFERENTIAL DIAGNOSIS — Parotid swelling has a wide differential diagnosis and includes conditions associated with sialadenosis, infectious causes, and neoplasm [30]. (See "Salivary gland swelling: Evaluation and diagnostic approach".)
Other causes of infectious parotitis — The main differential within infectious causes is non-suppurative parotitis that can be caused by a variety of viruses (mumps, influenza virus, coxsackievirus, Epstein-Barr virus, cytomegalovirus, parainfluenza viruses, herpes simplex virus (HSV), HIV, SARS-CoV-2, chronic hepatitis C virus, and lymphocytic choriomeningitis virus) [17,31].
In contrast with suppurative parotitis, viral parotitis is often bilateral and does not cause a purulent discharge from Stensen's duct [17]. It may also be distinguished from suppurative parotitis by its prodromal period followed by acute swelling of the involved gland, which can last 5 to 10 days. Bilateral parotid swelling with cystic lesions have been reported in patients with HIV; this is thought to be due either to HIV-associated sialadenitis or immune reconstitution inflammatory syndrome following initiation of antiretroviral therapy [32,33]. Chronic hepatitis C infection has also been associated with parotid abnormalities, such as lymphocytic sialadenitis and Sjögren's disease [34]. Serologic evaluation (eg, mumps, Epstein-Barr virus, cytomegalovirus, HIV) and polymerase chain reaction (PCR) of expressed secretions from Stenson's duct (eg, HSV PCR) can help establish the diagnosis.
●Mumps – Mumps is the classic virus to cause parotitis. It can be distinguished from suppurative parotitis by the presenting age of the patient, presence of a prodromal period, and presence of leukopenia instead of leukocytosis. Mumps typically occurs in children aged two to nine years of age, in contrast to suppurative parotitis, which typically is seen in infants under the age of one or in hospitalized adults. The prodromal period associated with mumps includes fever, headache, and malaise prior to the onset of parotid swelling. In addition, although mumps can initially present with unilateral parotitis, swelling extends bilaterally in 90 percent of infected individuals over the course of a few days. (See "Mumps", section on 'Clinical manifestations'.)
Noninfectious parotitis — There are numerous noninfectious causes of parotid swelling [17]. In general, these noninfectious causes should be considered if the swelling is painless, there is no purulent drainage from Stensen’s duct, and no systemic signs of toxicity are present. Most of these can be distinguished from suppurative parotitis based on imaging findings.
●Sialolithiasis – Sialolithiasis can cause recurrent episodes of unilateral parotid swelling that mimic suppurative parotitis [24]. The swelling may be painful or painless; however, there should be no purulent drainage from Stensen’s duct. If pain is present, it is typically associated with eating. Fever is uncommon. Ultrasound and noncontrast computed tomography (CT) imaging can help detect salivary stones during evaluation. (See "Salivary gland stones", section on 'Clinical features'.)
●Systemic disorders – Alcoholism, diabetes mellitus, and uremia can all cause parotid swelling. Onset of swelling is typically more indolent compared with the sudden onset in suppurative parotitis and other complications of the diseases are generally seen.
●Drug effects – Certain drugs can interrupt or diminish the flow of saliva through the parotid gland (eg, anticholinergics, antihistamines), leading to parotid inflammation and in some cases, suppurative parotitis. In the absence of purulent drainage, cessation of the culprit drug may be sufficient to resolve the symptoms. (See "Anticholinergic poisoning", section on 'Range of peripheral and central signs of toxicity'.)
●Tumors – Tumors of the parotid gland are rare. The tumor typically presents with a focal mass or subacute, unilateral, painless swelling of the parotid gland. There is no purulent drainage present in these cases and symptoms generally persist despite antibiotic therapy. Imaging with CT or magnetic resonance imaging (MRI) is often necessary to make the diagnosis. (See "Salivary gland tumors: Epidemiology, diagnosis, evaluation, and staging".)
Other noninfectious causes of parotid swelling include cystic fibrosis, gout, collagen vascular diseases, and sarcoidosis; these disorders rarely present with isolated parotitis and diagnosis is usually made based on a constellation of symptoms.
Rare causes of parotid swelling include radiation sialadenitis, ectodermal dysplasia syndromes, and familial dysautonomia.
Swelling outside of the parotid gland — Occasionally, swelling outside of the parotid gland may mimic parotitis; causes of swelling can include dental abscess, external otitis, cervical adenitis, infected cysts, and lymphoma [17]. CT or MRI will exclude these causes.
TREATMENT
Initial management and site of care — Initial treatment should be in an inpatient setting, since suppurative parotitis may spread to deep fascial spaces of the head and neck and can be life threatening. Initial management in the inpatient setting allows for aggressive hydration, administration of intravenous (IV) antibiotics, and prompt imaging. If there is no clinical response after 48 hours of treatment with empiric intravenous antibiotics, repeat imaging and cultures should be obtained and empiric therapy broadened. (See 'Managing poor clinical response or recurrence' below.)
There are no systematic data to inform the selection of an antibiotic regimen for the treatment of acute bacterial suppurative parotitis. Empiric regimen selection is based on the expected microbiology known to cause suppurative parotitis.
Community-acquired infection in immunocompetent patients
Initial empiric regimens — Initial empiric antimicrobial regimens are based upon the expected microbiology and patient factors and should be directed against methicillin-susceptible S. aureus, H. influenzae, viridans streptococci and other streptococci, and oral anaerobes (including Fusobacterium species) in immunocompetent patients with community-acquired infection. We do not routinely add therapy against methicillin-resistant S. aureus (MRSA) unless the patient has risk factors for it (table 1).
In immunocompetent patients with a community-acquired infection, we suggest (table 2):
●Ampicillin-sulbactam (3 g IV every six hours)
OR
●Cefuroxime (1.5 g IV every eight hours) or ceftriaxone (1 g IV every 24 hours) or levofloxacin (500 mg IV or orally every 24 hours)
plus
Metronidazole (500 mg IV or orally every eight hours) or clindamycin (600 mg IV or orally every six to eight hours)
If the patient is known to be colonized with MRSA or has risk factors for MRSA (table 1), we also add one of the following:
●Vancomycin (table 3), linezolid (600 mg orally or IV every 12 hours), or daptomycin (6 mg/kg IV every 24 hours)
Oral step-down regimens — Once the patient has improved (afebrile, reduced pain and swelling), the initial parenteral regimen can be transitioned to an oral regimen. If cultures have not been obtained, empiric oral regimens should include the same spectrum of pathogens as initial parenteral regimens (eg, staphylococci, H. influenzae, and oral aerobes and anaerobes). If microbiologic data are available and identify pathogens not treated by the initial regimen, the oral regimen should be broadened to include them; however, we continue to treat oral aerobes and anaerobes, even if these are not isolated. If MRSA does not grow on culture, treatment against MRSA can be discontinued.
Recommended empiric oral step-down regimens include (table 2):
●Amoxicillin-clavulanate (875/125 mg orally twice daily)
●Cefuroxime (500 mg orally every 24 hours) plus metronidazole (500 mg orally every eight hours)
●Levofloxacin (500 mg orally every 24 hours) plus metronidazole (500 mg orally every eight hours)
●Moxifloxacin (400 mg orally once daily) [35,36]
If therapy against MRSA is indicated, we also add one of the following:
●Linezolid (600 mg orally twice daily) or trimethoprim-sulfamethoxazole (1 double-strength tablet orally every 12 hours)
Hospital-acquired infections or immunocompromised patients
Initial empiric therapy — The expected microbiology is broader for immunocompromised patients or patients with a hospital-acquired infection. Initial empiric antimicrobial regimens should be directed against staphylococci (including MRSA), H. influenzae, viridans streptococci and other streptococci, oral anaerobes (including Fusobacterium species), Enterobacterales, and P. aeruginosa.
In these patients, we suggest (table 2):
Vancomycin (table 3) or linezolid (600 mg orally or IV every 12 hours) or daptomycin (6 mg/kg IV every 24 hours)
PLUS
One of the following regimens:
•Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV or orally every eight hours) or
•Piperacillin-tazobactam (4.5 g IV every six hours) or
•Imipenem (500 mg IV every six hours) or
•Meropenem (1 g IV every eight hours)
Oral step-down therapy — Once the patient has improved (afebrile, reduced pain and swelling), the initial parenteral regimen can be transitioned to an oral regimen. If cultures have not been obtained, empiric oral regimens should include the same spectrum of pathogens as initial parenteral regimens (eg, MRSA, H. influenzae, oral aerobes and anaerobes, Enterobacterales, and P. aeruginosa). If microbiologic data are available and identify pathogens not treated by the initial regimen, the oral regimen should be broadened to include them; however, we continue to treat oral aerobes and anaerobes, even if these are not isolated. If MRSA or P. aeruginosa do not grow on culture, treatment against these pathogens can be discontinued. (See 'Oral step-down regimens' above.)
Recommended empiric oral step-down regimens include (table 2):
●Levofloxacin (750 mg orally every 24 hours) plus metronidazole (500 mg orally every eight hours)
The following regimens also include anti-MRSA activity, if appropriate:
●Clindamycin (450 mg orally three times daily) plus ciprofloxacin (750 mg orally twice daily). MRSA susceptibility to clindamycin should be documented if this regimen is used for anti-MRSA therapy.
or
●Linezolid (600 mg orally twice daily) plus ciprofloxacin (750 mg orally twice daily) plus metronidazole (500 mg orally every eight hours).
or
●Trimethoprim-sulfamethoxazole (1 double-strength tablet orally twice daily) plus ciprofloxacin (750 mg orally twice daily) plus metronidazole (500 mg orally every eight hours).
Duration — There are no data available to guide duration of therapy for suppurative parotitis. Our approach is to determine duration based on severity and extent of infection and response to therapy. For patients with uncomplicated suppurative parotitis who have good clinical response, a total duration of 10 to 14 days is reasonable. If complications are present (eg, osteomyelitis, septic thrombophlebitis, bacteremia), duration should be determined by typical antibiotic duration therapy for that specific syndrome.
Managing poor clinical response or recurrence — If there is no improvement on empiric antibiotic therapy within 48 hours, repeat imaging and cultures should be obtained and empiric therapy broadened (eg, include therapy against MRSA and resistant gram-negative bacilli). If a parotid abscess is present, the abscess should be drained and aspirates sent for culture. Occasionally, surgical exploration and drainage may be required both to confirm the diagnosis and for management if clinical response is not optimal after 10 to 14 days of treatment.
In rare instances where recurrent suppurative parotitis occurs, every effort should be made to determine the etiology, including obtaining cultures with each recurrence and maintaining broad-spectrum antibiotic therapy if cultures are unrevealing. If the patient responds to antibiotics, a longer course may be necessary to fully eradicate any pathogens and prevent recurrence. In patients with recurrent parotitis despite appropriate treatment of infectious etiologies, computed tomography and/or magnetic resonance imaging should be pursued to evaluate for an underlying noninfectious etiology (malignancy or collagen vascular disease). In rare cases, a parotidectomy may be considered. (See "Parotidectomy".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topic (see "Patient education: Parotitis (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology and pathogenesis − Acute bacterial suppurative parotitis is an uncommon infection that occurs when salivary stasis allows oral flora to seed Stensen's duct (figure 1). It primarily occurs in infants under the age of one and in hospitalized older adults who are dehydrated or intubated. (See 'Epidemiology and risk factors' above.)
●Microbiology − Common causes include Staphylococcus aureus, oral aerobes and anaerobes, and Haemophilus influenzae. In hospital-acquired infections and in immunocompromised patients, methicillin-resistant S. aureus (MRSA), Enterobacterales, and Pseudomonas aeruginosa can also be seen. Parotitis can also be polymicrobial. (See 'Microbiology' above.)
●Clinical presentation – Patients present with sudden onset of unilateral firm, tender, and erythematous swelling over the parotid gland. Associated symptoms include fever, chills, trismus, dysphagia, and purulent drainage from the parotid duct. (See 'Clinical manifestations' above.)
●Complications – These include parapharyngeal space infection with airway compromise (figure 2), parotid abscess, septic jugular thrombophlebitis, osteomyelitis of the mandible, bacteremia, facial nerve palsy, and fistulas to the skin. (See 'Complications' above.)
●Diagnosis – The diagnosis is made in a patient with characteristic clinical findings (acute parotid swelling with purulent drainage from Stensen’s duct) and a diffusely enlarged gland with or without abscess on imaging (typically ultrasound). Lack of systemic symptoms (eg, fever) or drainage within the oral cavity does not exclude suppurative parotitis. Subacute progression of symptoms suggests a parotid abscess or extension of the infection into deeper tissues (eg, osteomyelitis). (See 'Approach to diagnosis' above.)
●Microbiologic evaluation − Purulent drainage from Stensen’s duct (picture 1) should be collected for Gram stain and culture. If abscess or underlying malignancy are suspected, ultrasound-guided fine needle aspiration should be obtained and sent to microbiology and cytology. (See 'Evaluation of microbiology' above.)
●Differential diagnoses – These include infectious causes (eg, mumps, influenza, coxsackievirus) and noninfectious causes (eg, sialolithiasis, tumors, drug side effects), as well as swelling outside of the parotid gland (eg, dental abscess, external otitis, or cervical adenitis). (See 'Differential diagnosis' above.)
●Initial treatment − Initial management includes hospitalization, aggressive hydration, and intravenous antibiotics directed against common pathogens. For initial empiric therapy of community-acquired infection in immunocompetent patients, we suggest a regimen with activity against staphylococci, H. influenzae, and oral aerobes and anaerobes (Grade 2C). For hospital-acquired infection and immunocompromised patients, we also include empiric therapy against MRSA, Enterobacterales, and P. aeruginosa. Example regimens are in the table (table 2). (See 'Initial management and site of care' above and 'Community-acquired infection in immunocompetent patients' above and 'Hospital-acquired infections or immunocompromised patients' above and 'Microbiology' above.)
●Oral step-down therapy and duration – Once the patient has improved, the antibiotic can be transitioned to an oral regimen, which should be informed by culture and susceptibility data (table 2). We typically maintain treatment against oral aerobes and anaerobes, even if they do not grow on culture. For patients with uncomplicated infection and good clinical response, we suggest 10 to 14 days of antibiotics (Grade 2C). Longer durations are appropriate for immunocompromised patients, slow response, or complications. (See 'Community-acquired infection in immunocompetent patients' above and 'Hospital-acquired infections or immunocompromised patients' above.)
●Poor clinical response − If there is no improvement on empiric antibiotic therapy within 48 hours, we repeat imaging, obtain repeat cultures, and broaden empiric therapy (eg, include therapy against MRSA and resistant gram-negative bacilli). Presence of abscess should prompt drainage. In settings of recurrent parotitis despite adequate antibiotic therapy, evaluation for noninfectious causes of parotitis should be pursued with advanced imaging. (See 'Managing poor clinical response or recurrence' above.)
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