Suppurative parotitis in adults

INTRODUCTION
1.

Acute infection of parotid gland can be caused by variety of bacteria and viruses. Acute
bacterial suppurative parotitis is caused most commonly by S. aureus and mixed oral aerobes
and/or anaerobes. It often occurs in setting of debilitation, dehydration, and poor oral
hygiene, particularly among elderly postoperative patients.
2. The epidemiology, clinical manifestations, microbiology, diagnosis, and treatment of
suppurative parotitis will be reviewed here. Deep neck space infections and salivary duct
stones are discussed separately.
ANATOMY AND PATHOGENESIS
1. The parotid glands are located on sides of face anterior to external auditory canal, superior to
angle of mandible, and inferior to zygomatic arch. Most of parotid gland is superficial to
masseter. The salivary gland consists of 20 to 30 intra-parotid and peri-parotid LN with
lymphatic drainage from ipsilateral side of face and forehead, including auricular region and
external auditory canal. Stensen's duct arises from anterior border of parotid gland and is 4 to
7 cm long; narrows to 1.2 mm at isthmus, and the os is 0.5 mm and is opposite upper second
molar.

2.

Acute bacterial suppurative parotitis may occur when salivary stasis permits retrograde
seeding of Stensen's duct by mixed oral flora. Ductal obstruction by calculi or tumor may
predispose to suppuration. Abscess formation may also arise by contiguous infection or
hematogenous seeding to intra-parotid or peri-parotid LN.

EPIDEMIOLOGY AND RISK FACTORS

1. Suppurative parotitis typically occurs in elderly post-operative patients who are dehydrated
or intubated, although it may also be seen in outpatients. Other predisposing factors include
recent intensive teeth cleaning, use of anti-cholinergic drugs and other drugs that reduce
salivary flow, malnutrition, salivary calculi with obstruction, and neoplasm of oral cavity.
Infection of embryogenic cysts, such as the first branchial cleft, may result in frequent
suppuration of the parotid gland.
CLINICAL MANIFESTATIONS
1. Suppurative parotitis is characterized by sudden onset of firm, erythematous swelling of preand postauricular areas that extends to angle of mandible. This is associated with exquisite
local pain and tenderness with complaints of trismus and dysphagia. Systemic findings of high
fevers, chills, and marked toxicity are generally present.
2.

On examination, fluctuant quality is not appreciated because of dense parotid fascia that
overlies gland. Purulent material may be expressed from orifice of Stensen's duct in over
one-half of cases.
MICROBIOLOGY
1. 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. G (-)
organisms (Enterobacteriaceae, Eikenella corrodens, and other GNB) are often seen in
hospitalized patients. For unexplained reasons, Klebsiella spp are particularly prevalent
among patients with DM from Southeast Asia.
2. The polymicrobial nature of parotid space infections was illustrated in study of 32 patients
with acute suppurative parotitis. Aerobic bacteria were isolated in 34%, anaerobic bacteria in
41%, and mixed aerobic and anaerobic bacteria in 25%. S. aureus was predominant aerobe,
followed by viridans streptococci and H. influenzae. Pigmented Prevotella and
Porphyromonas spp, Fusobacterium spp, and Peptostreptococcus spp were predominant
anaerobes.
3. Rare causes of suppurative parotitis include S. pneumoniae, S. pyogenes, M. catarrhalis,
Enterobacteriaceae spp, P. aeruginosa, M. tuberculosis, and Actinomyces spp.
IMAGING
1. Imaging studies are useful to assess for inflammation or duct obstruction by stone, and to
differentiate between acute suppurative parotitis and frank abscess collection or solid tumor.
Imaging options include ultrasound, CT, and MR sialography. On ultrasound, abscess
collection may be seen as hypo-echogenic lesion surrounded by irregular echogenic rim
within gland parenchyma. Ultrasound is particularly useful for detecting stones in duct or
parenchyma, or for differentiating between obstructive and non-obstructive sialoadenitis. CT
is most sensitive tool for differentiating suppurative cellulitis from frank abscess with rim
enhancement. X-ray sialography is also available, but cannot be used during acute infection
and requires the injection of contrast material.

DIAGNOSIS
1. The diagnosis is usually made when characteristic clinical findings are present, as discussed
above. An elevated serum amylase in absence of pancreatitis supports clinical suspicion of
parotid involvement. When purulent drainage is present at opening of Stensen's duct, it
should be collected for Gram stain and culture. Gram stain is particularly helpful in detecting
staphylococci and Candida. Culture obtained intra-orally, however, should be interpreted
with caution since the results may represent contamination by oral flora. Needle aspiration of
swollen parotid gland by extra-oral route is the best method to identify causative organisms.
Specimens should be cultured for both aerobes and anaerobes, as well as fungi and
mycobacteria. The primary utility of culture data is to obtain susceptibility testing of
dominant organism in order to ensure adequate antibacterial coverage.
TREATMENT
1.

2.

Treatment of suppurative parotitis includes hydration and IV antibiotics. Since suppurative

parotitis may potentially spread to deep fascial spaces of head and neck and is potentially
life-threatening, outpatient management with oral antibiotics is not advised. Surgical incision
and drainage should be implemented if there is no clinical response after 48 hours of
treatment with empiric intravenous antibiotics.
Initial antibiotic regimens
A. Initial empiric antimicrobial regimens are based upon expected microbiology and host
factors and should be directed at S. aureus (including MRSA) and mixed oral aerobes
and anaerobes. Additional coverage for Enterobacteriaceae and P. aeruginosa should be
considered in patients with prior hospitalization or who are immunocompromised. The
spectrum of antimicrobial regimen should be narrowed once microbiologic data become
available.
B. The antibiotic doses recommended below are intended for patients with normal renal
function; dosing of some of these agents must be reduced in patients with renal
dysfunction.
C. Immunocompetent hosts
i.
Nafcillin (1.5 g IV Q4H) or anti-staphylococcal penicillin or 1st cephalosporin plus
either
ii.
Metronidazole (500 mg IV Q6H) or clindamycin (600 mg IV Q6H)
iii.
Vancomycin (15 to 20 mg/kg IV Q12H) or linezolid (600 mg orally or IV Q12H)
should be substituted for nafcillin in immunocompetent host with risk factors for
MRSA infection. Risk factors for MRSA include history of IVD, comorbid disease
(DM), or residing in community or hospital where there is substantial incidence of
MRSA.

D.

3.

4.

Immunocompromised hosts
i.
Vancomycin (15 to 20 mg/kg IV Q8H, not exceed 2 g per dose) or linezolid (600 mg

orally or IV Q12H) plus one of following regimens.

1. Cefepime (2 g IV Q12H) plus metronidazole (500 mg IV Q6H)
2. Imipenem (500 mg IV Q6H)
3. Meropenem (1 g IV Q8H)
4. Piperacillin-tazobactam (4.5 g IV Q6H)
Oral step-down regimens
A. Step-down therapy to an oral regimen may be considered once the patient has improved
and surgical management is deemed unnecessary (table 1). The choice of an oral
antimicrobial regimen for step-down therapy should ideally be guided by culture and
susceptibility data. A combination of clindamycin (450 mg orally three times daily) plus
ciprofloxacin (500 or 750 mg orally twice daily) may be used to cover oral aerobes
(including Enterobacteriaceae spp), Pseudomonas aeruginosa, many strains of
Staphylococcus aureus, and anaerobes; the higher dose of ciprofloxacin should be used
when P. aeruginosa is suspected. An alternative regimen that does not have
anti-Pseudomonas activity is amoxicillin-clavulanate (875 mg BID) with or without
linezolid (600 mg BID); linezolid should be included if MRSA is suspected. Another
possible regimen is linezolid plus moxifloxacin (400 mg orally once daily), which provides
activity against oral aerobes (including Enterobacteriaceae spp), S. aureus, and
anaerobes, but does not have good activity against Pseudomonas aeruginosa.
Duration
A.

The duration of therapy depends upon the host immune status, severity and extent of
infection, and response to therapy. For patients with uncomplicated suppurative
parotitis, total duration of 10 to 14 days is reasonable.
COMPLICATIONS
1. Progression of infection may lead to massive swelling of neck, respiratory obstruction,
septicemia, and osteomyelitis of adjacent facial bone. Since parotid space abuts the
parapharyngeal space, suppurative parotitis is important source of parapharyngeal space
infection with potential for septic jugular thrombophlebitis. Another potential complication is
facial nerve palsy, which is relatively rare. Rarely, fistula may occur as complication of acute
suppurative parotitis. CT sialography and fistulography can be performed to evaluate extent
of fistula and to exclude possibility of underlying malignancy. A fistulectomy may be required
2.

for definitive management.

Surgical exploration and drainage may be required both for diagnosis and therapy. If an
infectious process is not found, a search for non-infectious causes of parotid swelling
(malignancy or collagen vascular diseases) should be made. In rare instances, recurrent
infection of the parotid gland may occur, particularly in patients with comorbid conditions,
such as DM. In such patients, parotidectomy may be considered.

NON-SUPPURATIVE CAUSES
1. A variety of organisms can cause parotitis. Mumps is classic virus to cause parotitis, but other
viruses that have been associated with parotitis include influenza, coxsackievirus, EBV,
lymphocytic choriomeningitis virus, parainfluenza viruses, HSV, and CMV.
2.

3.

Viral parotitis may be distinguished from suppurative parotitis by prodromal period, followed
by acute swelling of involved gland, which can last 5 to 10 days and is often bilateral. Viral
parotitis does not cause purulent discharge from Stensen's duct. Serologic evaluation can
establish diagnosis.
M. tuberculosis and NTM, such as M. avium intracellulare, have rarely been associated with
parotitis. HIV infection can cause bilateral non-suppurative parotitis.

4.

Non-infectious causes of parotid swelling include collagen vascular diseases, cystic fibrosis,
alcoholism, DM, gout, uremia, sarcoidosis, ectodermal dysplasia syndromes, familial

dysautonomia, sialolithiasis, benign and malignant tumors, and drug-related disorders.

SUMMARY AND RECOMMENDATIONS
1. Suppurative parotitis is caused most commonly by Staphylococcus aureus, but can also be
caused by oral aerobes and/or anaerobes. It often occurs in the setting of dehydration,
particularly among elderly postoperative patients.
2. Suppurative parotitis is characterized by the sudden onset of firm, erythematous swelling of
the pre- and postauricular areas that extends to the angle of the mandible. This is associated
with exquisite local pain and tenderness with complaints of trismus and dysphagia. Systemic
findings of high fevers, chills, and marked toxicity are generally present.
3. On examination, a fluctuant quality is generally not appreciated because of the dense parotid

4.

5.

6.

7.

8.

9.

fascia that overlies the gland. Purulent material may be expressed from the orifice of
Stensen's duct.
The microbiologic etiology of parotid space infections is most commonly polymicrobial. The
most common pathogens associated with acute bacterial parotitis are S. aureus, viridans
streptococci, and oral anaerobic bacteria.
The diagnosis is usually made when the characteristic clinical findings are present. When
purulent drainage is present at the opening of the duct of Stensen, it should be collected for
Gram stain and culture. However, the results should be interpreted with the knowledge that
oral flora may be contaminating the culture.
Treatment of suppurative parotitis includes hydration and intravenous antibiotics directed
against staphylococci and oral flora. The appropriate regimen depends on the immune status
of the patient and risk factors for MRSA. Risk factors for MRSA include a history of intravenous
drug use, comorbid disease (diabetes mellitus), or residing in a community or hospital where
there is a substantial incidence of MRSA.
For immunocompetent patients without risk factors for MRSA, one of the following regimens
provides appropriate coverage.
A. Nafcillin (1.5 g IV every four hours) or another antistaphylococcal penicillin or a
first-generation cephalosporin plus either
B. Metronidazole (500 mg IV every six to eight hours) or clindamycin (600 mg IV every six to
eight hours)
For immunocompetent patients with risk factors for MRSA, we suggest that vancomycin (15
to 20 mg/kg IV every 12 hours) or linezolid (600 mg orally or IV every 12 hours) be substituted
for nafcillin in the above regimen.
For immunocompromised patients, we suggest using a regimen that includes MRSA
coverage.

10. Appropriate regimens for immunocompromised patients include:

A. Vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or
linezolid (600 mg orally or IV every 12 hours) plus one of the following regimens:
B. Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every six to eight hours)
or
C. Imipenem (500 mg IV every six hours) or
D. Meropenem (1 g IV every eight hours) or
E. Piperacillin-tazobactam (4.5 g IV every six hours)
11. Step-down to an oral regimen may be considered once the patient has improved and surgical
management is deemed unnecessary. The choice of oral antimicrobial regimen for step-down
therapy should ideally be guided by culture and susceptibility data.
12. The duration of therapy depends upon the host immune status, severity and extent of
infection, and response to therapy. For patients with uncomplicated suppurative parotitis, a
total duration of 10 to 14 days is reasonable.