Infections caused by anaerobic bacteria are common, and may be serious and life-threatening. Anaerobes predominant in the bacterial flora of normal human skin and mucous membranes, and are a common cause of bacterial infections of endogenous origin. Infections due to anaerobes can evolve all body systems and sites. The predominate ones include: abdominal, pelvic, respiratory, and skin and soft tissues infections. Because of their fastidious nature, they are difficult to isolate and are often overlooked. Failure to direct therapy against these organisms often leads to clinical failures. Their isolation requires appropriate methods of collection, transportation and cultivation of specimens. Treatment of anaerobic bacterial infection is complicated by the slow growth of these organisms, which makes diagnosis in the laboratory only possible after several days, by their often polymicrobial nature and by the growing resistance of anaerobic bacteria to antimicrobial agents.

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Deep Head and Neck Infections ( Peritonsillar, Retro and Parapharyngeal Abscesses, Cervical Lymphadenitis, and Sialadenitis


 Peritonsillar, retropharyngeal and parapharyngeal abscesses are deep neck infections that are usually secondary to contiguous spread. They share similar clinical features, and also present with distinctive manifestations and complications (Table 1). When not recognized early, they are potentially life threatening. 


The microbiology of deep neck abscesses is similar because the causing bacteria reflect the host's oropharyngeal flora. Most oro-pharyngeal abscesses are polymicrobial; the average number of isolates is 5 (range 1 to 10).1-5 Predominant anaerobic organisms isolated in peritonsillar, lateral pharyngeal,  and retropharyngeal abscesses are Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus spp.; aerobic organisms are group A beta hemolytic streptococcus ( GABHS or Streptococcus pyogenes), Staphylococcus aureus and Haemophilus influenzae. Anaerobes are isolated from most abscesses whenever appropriate techniques for their cultivation have been employed while GABHS  is isolated in only about one-third of cases.1  Elevated antibody levels to Fusobacterium nucleatum and Prevotella intermedia, known oral pathogens was found in children who had peritonsillar abscess or cellulitis, supporting their pathogenic role.6
 More than two-thirds of deep neck abscesses contain beta-lactamase producing organisms.3,4 Retropharyngeal cellulitis and abscess in young children is more likely to have pathogenic aerobic isolates (streptococcus, S. aureus), alone or mixed.7 Fusobacterium necrophorum is especially associated with deep neck infections that cause septic thrombophlebitis of great vessels and metastatic abscesses (Lemierre disease).8 Rarely, Mycobacterium tuberculosis, atypical mycobacteria or Coccidioidis immitis  is recovered.

Obtaining appropriate specimens for cultures from the abscesses is important.  Specimens are best collected at the time of surgical drainage or through needle aspiration. 

Peritonsillar abscess

CT of peritonsillar abscess


 Surgical drainage of an abscess is the therapy of choice. However, administration of antimicrobial agents is also required. Because of their similar microbiology, the management of these abscesses is not different. Early initiation of antimicrobial therapy at the stage of cellulites can prevent abscess formation. Whe an abscess is diagnosed, antimicrobial therapy should be given and the abscess must be drained. Because of the risk of recurrence, tonsillectomy is performed six to eight weeks later. However, this is not always needed in children where recurrence rate is 7%, compared to 16% in adults. Controversy exists regarding management of peritonsillar abscess on an outpatient basis, after needle aspiration of the abscess. 9  
 The isolation of aerobic and anaerobic beta-lactamase-producing organisms (BLPO) from most abscesses mandates the use of antimicrobial agents effective against these organisms. BLPO include Prevotella, Fusobacterium, Haemophilus and Staphylococcus spp. 
 Efficacy antimicrobial agents include cefoxitin, a carbapenem (i.e., imipenem or meropenem), the combination of a penicillin (i.e., ticarcillin) and a beta-lactamase inhibitor (i.e., clavulanate), or clindamycin.


 Abscesses can rupture spontaneously into the pharynx leading to aspiration. Asphyxia can result from laryngeal edema, direct pressure, sudden abscess rupture and hemorrhage. Others include bacteremia, aspiration pneumonia, lung abscess,  lateral extension, or dissection into the posterior mediastinum and the prevertebral space.

Table 1: Clinical Features of Peritonsillar, Retropharyngeal & Lateral Pharyngeal Abscesses

Usual Age

Sites of Origin


Clinical Findings

Extension Site


Peritonsillar Abscess
Adolescents, adults
Tonsillar capsule, & space below superior constrictor muscle
Swelling of one tonsil, uvullar displacement; trismus, muffled voice
Spontaneous rupture & aspiration; contiguous spread to pterygomaxillary space
Antibiotics, drainage
Retropharyngeal Abscess
<4 years
Pharyngitis, dental infection trauma
Between posterior pharynx & prevertebral fascia
Unilateral posterior pharyngeal bulging; neck, hyperextension drooling, respiratory distress
Spontaneous rupture & aspiration; contiguous spread to posterior mediastinum, parapharyngeal space
Antibiotics, drainage; artificial airway
Lateral Pharyngeal Abscess
>8 adolescents, adults
Tonsillitis ottitis media, mastoiditis, parotitis, dental manipulation
Anterior & posterior pharyngomaxillary space
Anterior compartment: swelling of the parotid area; trismus; tonsil prolapse/tonsillar fossa
Posterior compartment: septicemia; minimal pain or trismus
Carotid erosion; airway obstruction; intracranium, lung, contiguous spread to mediastinum; septice


Cervical lymphadenitis (CL) is characterized by an inflammation of one or more lymph nodes in the neck.10 Usually involved lymph nodes are the anterior cervical, the submandibular, or the posterior cervical. An immunologic process without local infection or certain malignancies may produce similar clinical picture.


The cervical lymphatic system is a first line of defense against upper respiratory tract, teeth or the soft tissues infections of the face and scalp.

 Viruses are the most common etiology of bilateral CL in children. 10 The most common viruses are Epstein-Barr, cytomegalovirus, herpes simplex, adeno virus, enterovirus, roseola, rubella and the human immunodeficiency virus (HIV). Other pathogens of CL include Mycoplasma pneumoniae and Corynebacterium diphtheriae. The most common bacterial organisms causing acute unilateral infection associated with facial trauma or impetigo are S. aureus and GABHS.10-12 Other causes include Bartonella henselae, Haemophilus influenzae, Francisella tularensis, Pasteurella multocida, Yersinia pestis, Yersinia entercolitica, Listeria monocytogenes, Actinobacillus actinomycetemcomitans, Burkholderia gladioli, Spirillum minor, Nocardia brasiliensis,  Mycobacterium tuberculosis, and non-TB mycobacterium13,14 Other rare aerobic pathogens are Streptococcus pneumoniae and Gram-negative rods. Adenitis in newborns is often associated with group B streptococci. 

 The most common fungi involved in CL are Histoplasma capsulatum, Coccidioides immitis, and Paracoccidioides spp.

 Studies that utilized methodologies that were adequate for the recovery of anaerobes demonstrated their importance in CL mostly in association with dental or periodontal disease. 11,12  The predominate anaerobes were Peptostreptococcus spp, Gram-negative bacilli and Fusobacterium spp.


Establishment of the infection's etiology is important whenever the infection does not resolve within a few days. Aspiration of the lesion may provide important clues. The aspirate should be inoculated for recovery of aerobic and anaerobic bacteria, fungi, and mycobacteria. Gram and acid fast strains should be done of the specimen. Intradermal skin test for tuberculosis and atypical mycobacteria should be applied. If no improvement occurs following antimicrobial therapy, additional studies need to be done. These include erythrocyte sedimentation rate, chest roentgenogram and serological tests for toxoplasmosis, Epstein-Barr (EB) and HIV viruses, cytomegalovirus, coccidioidomycosis, histoplasmosis, tularemia, brucellosis and syphilis. PCR methodology can be used for rapid detection of Mycobacteria. If the diagnosis remains unclear, excision biopsy should be done. This should be submitted for the above studies as well as viral cultures, histology, Giemsa, periodic acid-Schiff, and methenamine silver stains. 


 The majority of patients with CL do not require specific therapy as they are a result of viral pharyngitis or stomatitis. Empiric antimicrobial therapy should provide adequate coverage for S. aureus and GABHS. Oral antimicrobial agents should include penicillinase-resistant penicillins such as cloxacillin, dicloxacillin, or the combination of a penicillin ( i.e. amoxicillin ) and a beta-lactamase inhibitor( i.e. clavulanic acid). Parenteral therapy may be required in toxic patients. Patients allergic to penicillin can be treated with a macrolide or clindamycin. Treatment should be administered for at least 14 days. Therapy against anaerobic and aerobic BLPO include clindamycin, the combination of a penicillin and a beta-lactamase inhibitor, or the combination of a penicillin or macrolide and metronidazole. If no improvement occurs after 36 to 48 hours of therapy a reassessment is required. Culture results may assist in the selection of therapy.

 Early institution of antibiotics prevents most cases of pyogenic adenitis from progressing to suppuration. However, once fluctuation occurs, antibiotics alone are generally not sufficient and the abscess should be incised and drained.

  When mycobacterial or cat-scratch disease is suspected, incision and drainage should be avoided as chronically draining cutaneous fistulae often develops.14 A large needle ( 18- or 19-gauge needle ) is preferred to avoid formation of a fistula. Therapy with rifampin, trimethoprim-sulfamethoxazole, or gentamicin should be considered in cat-scratch disease directed at B. henselae. Total surgical removal is most effective therapy for nontuberculous mycobacterial CL. Therapy with antimycobacterial therapy is generally initiated until the organisms are identified as atypical mycobacteria. This includes the administration of rifampin and isoniazid. When atypical mycobacteria are recovered these drugs are generally stopped; however, therapy is continued for 9 to 12 months if M. tuberculosis is identified. 


Complications include cellulitis, bacteremia, sepsis, toxin-related symptoms (in case of streptococci or staphylococci), internal jugular vein thrombosis, pulmonary emboli or disseminated septic emboli, mediastinitis and pericarditis. 


Infections of the thyroid are rare, but potentially life threatening.15 The signs and symptoms of infectious thyroiditis may mimic those of a variety of noninfectious inflammatory conditions.


S. aureus, S. pyogenes, Streptococcus epidermidis, and S. pneumoniae, are the predominant aerobic isolates. The most common anaerobic bacteria are Gram-negative bacilli, Peptostreptococcus spp. and  Actinomyces spp.15-17 

 Agents that are rarely recovered include Klebsiella spp., Haemophilus influenzae, Streptococcus viridans, Salmonella spp., Enterobacteriaceae, Mycobacterium tuberculosis, atypical mycobacteria, Aspergillus spp., Coccidioides immitis, Candida  spp., Treponema pallidum, and Echinococcus spp. Viruses  associated with subacute thyroiditis are measles, mumps, influenza, enterovirus Epstein-barr, adenovirus, echovirus, and St. Louis encephalitis.


The sources of thyroid infection are: hematogenous, direct spread from a adjacent site,  a thyroglossal cyst or fistula, or a through perforated esophagus. Preceding conditions include: goiter or thyroid adenomata, pharyngitis, immune-deficiency,  HIV  infection, leukemia, gastroenteritis, pyelonephritis, dental infections, brain abscess, otitis, mastoiditis, glositis, pulmonary infection, postpartum sepsis, erysipelas, subphrenic or pilonidal abscess, and malignancy in the vicinity of the thyroid gland.


 Acute ST is characterized by a sudden onset of pain, and firm, tender, red, warm swelling in the anterior neck that moves on swallowing and develops over days to a few weeks with or without fever, tenderness, local warmth, erythema, hoarseness, dysphagia, dysphonia, and concurrent pharyngitis.15 Other signs include involuntary depression of the chin upon swallowing and limitation of cervical extension.

 ST should be differentiated from other more common thyroid conditions such as adenoma or goiter. Subacute thyroiditis usually subsides over time, whereas untreated ST generally results in increasing toxicity.18 Other conditions that need to be differentiated from ST are intracystic hemorrhage, malignancy and rarely painful Hashimoto’s thyroiditis. Serum thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) are generally normal. Hypothyroidism is seen in about half of the patients.

 Sonography assists in the differentiation of ST from other causes of anterior neck pain and fever and allows radiographically-guided drainage of a thyroid abscess. Thyroid radionuclide scanning may not always visualize the organ with diffuse inflammation, although "patchy" uptake or a "cold" area can be present with localized or less severe involvement. Plain roentgenograms can detect free gas in the tissues produced by gas-forming bacteria, or the presence of calcifications associated with Echinococcus or Pneumocystis infection. The presence of soft-tissue gas and foul-smelling pus suggests the presence of an anaerobic infection.

  Needle aspiration can facilitate the diagnosis and choice of proper antimicrobials.15 The aspirate should be inoculated for recovery of aerobic and anaerobic bacteria, fungi, and mycobacteria and processed for Gram and acid fast strains. Intradermal skin test for tuberculosis and atypical mycobacteria should be applied.


 A broad coverage of antimicrobial agents is indicated, at least until culture results are available. Empiric antimicrobial therapy should cover S. aureus and S. pyogenes. Oral antimicrobials should include penicillinase-resistant penicillins (ie dicloxacillin) or the combination of a penicillin ( i.e. amoxicillin ) and a beta-lactamase inhibitor ( i.e. clavulanic acid). Parenteral therapy may be required in toxic patients. Patients allergic to penicillin can be treated with a macrolide or clindamycin. Treatment should be administered for at least 14 days.

  Early institution of treatment with antibiotics can prevent most cases of ST from progressing to suppuration. However, once fluctuation occurs, antibiotic therapy alone is generally not sufficient.

 Surgical drainage is indicated when antibiotic therapy fails to control the infection. If extensive necrosis or persistence of infection in spite of antibiotics is demonstrated, lobectomy may be required.15,18


 Complications are rare and include vocal cord paralysis, pericarditis, abscess rupture or extension into adjacent sites and organs (anterior mediastinum, trachea, esophagus), thrombosis of the internal jugular vein (Lemiere's syndrome), and extrinsic compression of the trachea, transitory hypothyroidism that requires replacement therapy, myxedema, disruption of regional sympathetic nerves, and recurrent infection.19


1. Brook, I., Shah, K.: Bilateral peritonsillar abscess: an unusual presentation. South. Med. J. 74:514-5, 1981.
2. Finegold, S.M.: Anaerobic bacteria in human disease. New York, Academic Press. 1977
3. Brook, I.: Microbiology of abscesses of the head and neck in children. Ann. Otol. Rhinol. Laryngol. 96:429-33, 1987.
4. Brook, I.: Aerobic and anaerobic bacteriology of peritonsillar abscess in children. Acta Paediatr Scand 70:831–8, 1981.
5. Brook, I.: Microbiology of retropharyngeal abscesses in children. Am J Dis Child 141:202–4, 1987.         
6. Brook, I., Foote, P.A .Jr., Slots, J.: Immune response to anaerobic bacteria in patients with peritonsillar cellulitis and abscess. Acta Otolaryngol 116:888–91, 1996.         
7. Asmar, B.I.: Bacteriology of retropharyngeal abscess in children. Pediatr Infect Dis J 9:595–6, 1990.
8. Hughes, C.E., Spear, R.K., Shinabarger, C.E., Tuna I.C.: Septic pulmonary emboli complicating mastoiditis: Lemierre's syndrome. Clin Infect Dis 18:633–5, 1994.
9. Wolf, M., Even-Chen, I., Kronenberg, J.: Peritonsillar abscess: repeated needle aspiration versus incision and drainage. Ann Otol Rhinol Laryngol 103:554–7, 1994.
10. Peters TR, Edwards KM. Cervical lymphadenopathy and adenitis. Pediatr Rev; 21:399-405, 2000.
11.  Brook, I.: Aerobic and anaerobic bacteriology of cervical adenitis in children. Clin. Pediatr. 19:693-5, 1980.
12. Brook, I., Frazier, E.H.: Microbiology of cervical lymphadenitis in adults. Acta Otolaryngol 118:443–6, 1998.
13. Graves, M., Robin, T., Chipman, A.M., Wong, J., Khashe, S., Janda, J.M.: Four additional cases of Burkholderia gladioli infection with microbiological correlates and review. Clin Infect Dis 25:838–42, 1997.
14. Hazra, R., Robson, C.D., Perez-Atayde, A.R., Husson, R.N.: Lymphadenitis due to nontuberculous mycobacteria in children: presentation and response to therapy. Clin Infect Dis 28:123-9, 1999.
15. Shah, S.S., Baum, S.B.: Infectious Thyroiditis: diagnosis and Management. Current Infect. Dis. Reports. 2; 147-53, 2000.
16. Jeng, L.B., Lin, J.D., Chen, M.F.: Acute suppurative thyroiditis: a ten year review in a Taiwanese hospital. Scan J Infect Dis 26:297-300, 1994.
17. Yu, E.H., Ko, W.C., Chuang, Y.C., Wu TJ.: Suppurative Acinetobacter baumanii thyroiditis with bacteremic pneumonia: case-report and review. Clin. Infect. Dis. 27:1286-1290, 1998.
18. Slatosky J, Shipton B, Wahba H : Thyroiditis: differential diagnosis and management. Am Fam Physician  61: 1047-52, 2000.
17. Guttler R, Singer PA, Axline SG, et a. Pneumocystis carinii thyroiditis. Report of three cases and review of the literature. Arch Intern Med.;153:393-6. 1993.
18. Spitzer RD, Chan JC, Marks JB, et al. Case report: hypothyroidism due to Pneumocystis carinii thyroiditis in a patient with acquired immunodeficiency syndrome. Am J Med Sci. ;302:98-100.1991.
19. Lough, D.R., Ramadan, H.H., Aronoff, S.C.: Acute suppurative thyroiditis in children. Otolarngol Head and Neck Surg 114:462-465, 1996.


Sialadenitis, an acute infection of the salivary glands can occur in any of the glands. The parotid gland is the salivary gland most commonly affected by inflammation, and most reports of the microbiology of sialadenitis were limited to this condition1. The microbiology of infection of the submandibular and sublingual glands has rarely been reported 2.

The parotid gland is the salivary gland most commonly affected by inflammation. Parotitis can present as an acute single, or multiple recurrent episodes. Acute suppurative parotitis may arise from a septic focus in the mouth, such as chronic tonsillitis or dental sepsis, and may be found in patients taking tranquilizer drugs or antihistamines, both of which tend to suppress saliva excretion.

It occurs mostly children younger than 2 month and in elderly persons who are debilitated by systemic illness or previous surgical procedures, although persons of all ages may be affected.1 Other predisposing factors include dehydration, immunosuppression, malnutrition, neoplasms of the oral cavity, tracheostomy, immunosuppression, sialectasis, ductal obstruction and medications that diminish salivary flow such as antihistamines and diuretics.2,3

The mode of spread of organisms into the parotid gland may be caused by combinations of factors that enhance ascention of oral bacteria through the stensens duct. These include following the decreased secretory function that occurs in the dehydrated or starving patient.3 Another possible mode of transmission of organisms is through transitory bacteremia especially in the neonatal period.


 Staphylococcus aureus is the most common pathogen associated with acute bacterial parotitis; however, streptococci (including Streptococcus pneumoniae) and Gram-negative bacilli (including Escherichia coli) have also been reported.1,2 Gram-negative organisms are often seen in hospitalized patients. Organisms less frequently found are Arachnia, Haemophilus influenzae, Treponema pallidum, cat-scratch bacillus, and Eikenella corrodens.4

 Mycobacterium tuberculosis and atypical mycobacteria are rare causes of parotitis.5 Several reports describe anaerobic isolates from parotid infections.6-14 However, the true incidence of anaerobic bacteria in suppurative parotitis is not yet determined because most past studies did not employ proper techniques for their isolation.

 Brook and Finegold reported two patients with acute suppurative parotitis11 In one case, the cultures yielded mixed culture of Prevotella intermedia and alpha-hemolytic streptococci. In the other child, no aerobes were recovered and the specimen yielded growth of Fusobacterium nucleatum and Peptostreptococcus intermedius. Of interest is that both of these patients were institutionalized mentally retarded children, and one had Down's syndrome. Notably, children with Down's syndrome have a striking incidence of severe periodontal disease and have a greater prevalence of Prevotella melaninogenica in the gingival sulcus in comparison with normal children.15

  Sussman recovered Gaffkya anaerobia from recurrently infected parotic gland.12 Actinomyces israelii and Actinomyces eriksonii also have been isolated.4,9

  We studied 23 aspirates of pus from acute suppurative parotitis for aerobic and anaerobic bacteria.16 A total of 36 bacterial isolates (20 anaerobic and 16 aerobic and facultative) were recovered, accounting for 1.6 isolates per specimen (0.9 anaerobic and 0.7 aerobic and facultative). Anaerobic bacteria only were present in 10 (43%) patients, aerobic and facultatives in 10 (43%), and mixed aerobic and anaerobic flora in 3 (13%). Single bacterial isolates were recovered in 9 infections, 6 of which were Staphylococcus aureus and 3 were anaerobic bacteria. The predominant bacterial isolates were S. aureus (8 isolates), anaerobic gram negative bacilli (6 isolates, including 4 pigmented Prevotella and Porphyromonas), and Peptostreptococcus sp. (5).

  Aspirates of pus from acute suppurative sialadenitis, were studied for aerobic and anaerobic bacteria. 17 Bacterial growth was present in a total of 47 specimens, 32 from parotid, 9 from submandibular, and 6 from sublingual glands specimens. A total of 55 isolates, 25 aerobic and 30 anaerobic were recovered from  parotid infection; anaerobic bacteria only were recovered in 13 (41%), aerobic or facultative bacteria only in 11 (34 %) and mixed aerobic and anaerobic bacteria were recovered in 8 (25 %). (Table 1) A total of 17 isolates, 8 aerobic and 9 anaerobic were recovered from submandibular gland infection; anaerobic bacteria only were recovered in 3 (33%) specimens, aerobic or facultative bacteria only in 4 (44 %) and mixed aerobic and anaerobic bacteria were recovered in 2 (22 %). A total of 10 isolates, 5 aerobic and 5 anaerobic were recovered from In sublingual gland infection; anaerobic bacteria only were recovered in 2 (33%) specimens, aerobic or facultative bacteria only in 2 (33 %), and mixed aerobic and anaerobic bacteria were recovered in 2 (33 %). The predominate aerobes was S. aureus and H.influenzae and the predominate anaerobes were gram negative bacilli (including pigmented Prevotella and  Porphyromonas, and Fusobacterium spp.)  and Peptostreptococcus  spp.  This study highlights the polymicrobial nature and importance of anaerobic bacteria in acute suppurative sialadenitis.
 There are two other reports of recovery of anaerobes from infections of other salivary glands. Bock18 described a patient with sublingual gland inflammation and a bad taste in the mouth. Numerous spirochetes and a few fusiform bacilli were seen on smears. Baba, et a 19 obtained a Peptococcus in pure culture from a purulent submaxillary gland infection.


  Although acute parotitis from anaerobic bacteria has been rarely reported, its occurrence should not be surprising. Both clinicopathologic correlations in humans and experimental studies in dogs have shown that bacteria can ascend Stensen's duct from the oral cavity and thus infect the parotid glands.20 Improved techniques for isolation and identification of anaerobic bacteria have shown that the flora of the mouth is predominantly anaerobic, and normal adults harbor about 1011 microorganisms per gram of material in gingival crevices.21 Saliva contains many genera of anaerobic bacteria, including Peptostreptococcus, Veillonella, Actinomyces, Propionibacterium, Leptotrichia, pigmented Prevotella and Porphyromonas spp., Bacteroides, and Fusobacterium. Diminution in salivary flow could allow the ascent of any of the indigenous bacterial flora, thereby triggering acute parotitis.4
 Pigmented Prevotella and Porphyromonas spp. are the most common anaerobic gram negative bacilli found in oral flora and, like Peptostreptococcus species, are frequently isolated from odontogenic orofacial infections.5 The paucity of reports of involvement of such organisms in bacterial infections of the parotid gland probably indicates that anaerobic cultures have not been done, or that inadequate anaerobic transport or culture techniques accounted for failure to recover such organisms.


Acute parotitis


 Acute suppurative parotitis is characterized by the sudden onset of an indurated, warm, erythematous swelling of the cheek extending to the angle of the jaw. Acute bacterial parotitis usually is unilateral, the gland becomes swollen and tender, and patients frequently have toxemia with marked fever and leukocytosis. The orifice of the parotid duct is red and pouting, and pus may be seen exuding, or may be produced by gentle pressure on the duct. Pus rarely points externally because of the dense fibrous capsule of the gland.

Pus coming out from the Stenon duct

  The pathogenic process associated with suppurative parotid infection may lead to profound dehydration, delirium, high fever, bacteremia, and organ system failure.
  Acute suppurative parotitis should be differentiated from viral parotitis (mumps), which usually is endemic and produces no pus. Other viruses that can cause parotitis include HIV, enteroviruses, Epstein-Barr-virus, parainfluenza, influenza, cytomegalo virus and lymphocytic choriomeningitis virus. Other noninfectious disorders that may be associated with parotid swelling include collagen-vascular disease, cystic fibrosis, alcoholism, diabetes, gout, uremia, sarcoidosis, ectodermal dysplasia syndromes, familial dysautonomia, sialolithiasis, benign and malignant tumors, metal poisoning drug related disorders. Nonparotid swelling that may stimulate parotitis include lymphoma, lymphangitis, cervical adenitis, external otitis, dental abscess, actinomyces not evolving the parotid, and cysts.
 Suppurative parotitis is differentiated from these disorders by the ability to produce purulent material at the orifice of Stensen duct by applying pressure over the gland. Occlusion of the orifice may, however, prevent the expression of pus. Tumors are generally unevenly swollen, and tenderness is variable.
 Anaerobic infection of the buccal space (such as Ludwig's angina) not evolving the parotid have to be differentiated from parotitis. Actinomyces may have chronic exudate with sulfur granules and is frequently encountered with dental caries. Elevated white blood cells and sedimentation rate and serum amylase or urine diastase are generally seen in suppurative parotitis. 

 Roentgenogram may reveal the presence of sialolith, and sialogram may demonstrate destruction of ductules or spherical dilation suggestive of suppurative illness.23 CT-sialography is an important tool in diagnosis of tumors.24

Left sialogram 

  Expression of the pus from the parotid gland and performance of Gram stain may support suppurative infection. Specimens for anaerobic culture should not be taken from Stensen's duct because oropharyngeal contamination is certain.

 Needle aspiration of the gland may yield the causative organism. If no pus is aspirated, introduction of sterile saline and subsequent aspiration may yield organisms. The aspirates should be cultured for aerobic as well as anaerobic bacteria, fungi, and mycobacteria. Surgical exploration and drainage may be indicated for diagnosis as well as for therapy. If infection is not found, search should be made for noninfectious causes of parotic swelling previously mentioned.


  Maintenance of adequate hydration and administration of parenteral antimicrobial therapy are essential. The choice of antibiotics depends on the etiologic agent. Most cases respond to antimicrobial therapy; however, some inflamed glands may reach a stage of abscess formation that requires surgical drainage. Broad antimicrobial therapy is indicated to cover all possible aerobic and anaerobic pathogens, including adequate coverage for S. aureus, hemolytic streptococci, and beta-lactamase producing anaerobic gram negative bacilli.

  A penicillinase-resistant penicillin or first-generation cephalosporin is generally adequate. However, the pressure of methicillin-resistant staphylococci may mandate the use of vancomycin. Clindamycin, cefoxitin, imipenem, the combination of metronidazole and a macrolyde or a penicillin plus beta-lactamase inhibitor, will provide adequate coverage for anaerobic as well as aerobic bacteria.

 Maintenance of good oral hygiene, adequate hydration, and early and proper therapy of bacterial infection of the oropharynx may reduce the occurrence of suppurative parotitis.


1.   Krippaehne, W.W., Hunt, T.K.,  Dunphy, J.E.: Acute suppurative parotitis: a study of 161 cases. Ann. Surg. 156:251-257, 1962.
2.   Petersdorf, R.G., Forsyth, B.R., Bernanke, D.: Staphylococcal parotitis. N. Engl. J. Med. 259:1250-1258, 1958.
3.   Guralnick, W.C., Donoff, R.B.,  Galdabini, J.: Tender parotid swelling in a dehydrated patient. J. Oral. Surg. 26:669-675, 1968.
4.   Brook, I.: Diagnosis and management of parotitis. Arch Otolaryngol Head Neck Surg. 118:469–71, 1992.
5.   Green PA, von Reyn CF, Smith RP Jr.. Mycobacterium avium complex parotid lymphadenitis: successful therapy with clarithromycin and ethambutol.  Pediatr Infect Dis J  12:615-7. 1993.
6.   Shevky, M., Kohn, C.,  Marshall, M.S.: Bacterium melaninogenicum. J. Lab. Clin. Med. 19:689-673, 1934.
7.   Heck, W.E.,  McNaught, R.C.: Periauricular Bacteroides infection, probably arising in the parotid. J.A.M.A. 149:662-3, 1952.
8.   Beigelman, P.M.,  Rantz, L.A.: Clinical significance of Bacteroides. Arch. Intern. Med. 84:605-31, 1949.
9.   Hensher R, Bowerman J Actinomycosis of the parotid gland.
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10. Anthes, W.H., Blaser, M.J.,  Reller, L.B.: Acute suppurative parotitis associated with anaerobic bacteremia. Am. J. Clin. Pathol. 75:260-262, 1981.
11. Brook, I., Finegold, S.M.: Acute suppurative parotitis caused by anaerobic bacteria: report of two cases. Pediatrics 62:1019-1020, 1978.
12. Sussman, S.J.: Gaffkya anaerobia infection and recurrent parotitis. Clin. Pediatr. 25:323-324, 1986.
13. Lewis, M.A., Lamey, P.J., Gibson, J.: Quantitative bacteriology of a case of acute parotitis. Oral Surg Oral Med Oral Pathol 68:571–5, 1989.
14. Guardia, S.N., Cameron, R., Phillips, A.: Fatal necrotizing mediastinitis secondary to acute suppurative parotitis. J Otolaryngol 20:54–6, 1991.
15. Meskin, L.H., Farsht, E.M., Anderson, D.L.: Prevalence of Bacteroides melaninogenicus in the gingival crevice area of institutionalized trisomy 21 and cerebral palsy patients and normal children. J. Periodontol. 39:326-328, 1968.
16. Brook, I., Frazier, E.H., Thompson, D.H.: Aerobic and anaerobic microbiology of acute suppurative parotitis. Laryngoscope 101:170–2, 1991.
17. Brook, I. :Aerobic and anaerobic supporative Sialadenitis. In press , Annals of Otolaryngology.
18. Bock, E.: Ueber isolierte Entzundung der Glandula sublingualis durch Plaut-Vincentsche Infektion. Munch. Med. Wochenschr. 85:786-88, 1938.
19. Baba, S., Mamiya, K.,  Suzuki, A.: Anaerobic bacteria isolated from otolaryngologic infections. Jpn. J. Clin. Pathol. 19 (suppl.):35-39, 1971.
20. Berndt, A.L., Buck, R., Buxton, R.L.: The pathogenesis of acute suppurative parotitis. Am. J. Med. Sci. 182:639-640, 1931.
21. Socransky, S.S.,  Manganiello, S.D.: The oral microbiota of man from birth to senility. J. Periodontal 42:485-496, 1971.
22. Finegold, S.M.: Anaerobic bacteria in human disease.  New York,  Academic Press. 1977.
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