ACP medicine, 3rd Edition

Infectious Disease

Bacterial Infections of the Upper Respiratory Tract

Harvey B. Simon MD, FACP1

Associate Professor of Medicine

1Harvard Medical School; Health Sciences and Technology Faculty, Massachusetts Institute of Technology; Physician, Massachusetts General Hospital

The author has no commercial relationships with manufacturers of products or providers of services discussed in this chapter.

June 2006

Overview of Upper Respiratory Tract Infections

Upper respiratory tract infections are the most common maladies experienced by humankind.1 They range from common, benign processes, such as nasopharyngitis, to uncommon, potentially lethal processes, such as epiglottitis. Pathogens range from pyogenic bacteria [see 7:I Infections Due to Gram-Positive Cocci and 7:II Tuberculosis] to Chlamydia [see 7:XIII Diseases Due to Chlamydia], mycoplasmas [see 7:XII Mycoplasma Infections], respiratory viruses [see 7:XXV Respiratory Viral Infections], and, on occasion, fungi [see 7:XXXVII Mycotic Infections]. Despite this heterogeneity, some general anatomic and physiologic principles apply.

PATHOPHYSIOLOGY

The upper respiratory tract is composed of two distinct types of epithelial surface. A stratified squamous epithelium lines the oropharynx and nasopharynx [see Figure 1]. These regions are normally teeming with a variety of microbial flora, and many potential pathogens can temporarily colonize these epithelial surfaces without causing true infection [see Table 1]. Bacteriologic cultures are easily obtained from these areas. As a result, the microbiology laboratory faces the challenge of isolating potential pathogens from the normal mouth flora, and the clinician faces the challenge of distinguishing between the carrier state and active infection. A respiratory epithelium, composed of ciliated columnar cells, goblet cells, and mucous and serous glands, lines the paranasal sinuses, the middle ear, and the airway below the epiglottis. These regions, in contrast to the oropharynx and nasopharynx, are normally sterile. Because these areas are inaccessible for routine culture, it is often necessary to diagnose and treat infections on the basis of clinical findings and statistical probabilities [see Table 1] rather than on the basis of bacteriologic data derived from an individual patient.

Table 1 Major Microbial Flora of the Upper Respiratory Tract

Organism

Oral Cavity

Nasopharynx, Tonsils

Epiglottis, Larynx

Paranasal Sinuses, Middle Ear

Gram-positive cocci

   Coagulase-negative staphylococci

NF

NF

 

UP

   S. aureus

 

CC

UP

UP

   Pneumococci

CC

UP

CP

   Group A streptococci

CC, CP

UP

CP

   Groups C and G streptococci

CC, UP

 

 

   Other streptococci

NF

NF

CP

Gram-positive bacilli

   Diphtheroids

NF

NF

 

 

   Corynebacterium diphtheriae

 

UC, UP

UP

   Arcanobacterium haemolyticum

 

 

Gram-positive anaerobes

   Anaerobic streptococci

NF

NF

 

UP*

   Anaerobic diphtheroids

NF

NF

 

   Actinomyces species

NF, UP

 

Gram-negative cocci

   Neisseria meningitidis

 

CC, UP

 

 

   N. gonorrhoeae

UC, UP

   Other Neisseria species

NF

NF

UP

   Moraxella catarrhalis

NF

NF

CP

Gram-negative coccobacilli

   Haemophilus influenzae

 

CC, UP

CP

CP

   Other Haemophilusspecies

NF

NF

 

 

Gram-negative bacilli

   Enterobacteriaceae

UC

UC

UP

 

   Pseudomonas aeruginosa

UC

UC

 

Gram-negative anaerobes

   Prevotella species

NF, UP

 

 

UP*

   Fusobacterium species

NF, UP

UP*

   Veillonella species

NF

 

Mycobacterium

   M. tuberculosis

UP

UP

UP

UP

Spirochetes

   Borrelia species

NF, UP

NF, UP

 

 

   Treponema pallidum

UP

UP

Fungi

   Candida albicans

NF

NF, UP

 

 

   Aspergillus species

 

 

UP

   Mucor species

UP

Chlamydophilia

   C. pneumoniae

 

UP

 

 

Mycoplasma

   M. pneumoniae

 

UC, UP

UP

UC, UP

Viruses

   Epstein-Barr virus

 

CP, CC

 

 

   Herpes simplex virus

CC, CP

UP

   Influenza virus

 

CP

CP

   Parainfluenza virus

CP

CP

   Adenovirus

CP, UC

CP

   Coxsackievirus

CP

CP

CP

   Rhinovirus

 

CP, UC

CP

   Respiratory syncytial virus

CP

CP

*Anaerobic bacteria predominate in the normal flora of the upper respiratory tract. They are uncommon pathogens in acute infections but are common pathogens in chronic sinusitis and otitis, as well as in abscesses, soft tissue infections, and periodontal infections; aerobic pathogens participate synergistically in most of these processes. CC — Common colonizer: organism present in many individuals, often transiently, without causing disease; CP — Common pathogen: organism frequently causes disease in this location; NF — Normal flora: organism present in most healthy individuals; UC — Uncommon colonizer: organism present without causing disease but relatively uncommon; UP — Uncommon pathogen: organism infrequently causes disease in this location.

 

Figure 1. Sagittal section through the nose, mouth, pharynx, and larynx.

Many host defense mechanisms protect the upper airway from infection. Mechanical defenses tend to prevent penetration of organisms from the nasopharynx and oral cavity into more vulnerable areas. These defenses are the cough, gag, and sneeze reflexes; the viscous mucous secretions, which entrap particulate material; and ciliary action, which propels entrapped particles outward. In addition, local immunologic defenses attempt to deal with organisms that have breached the mechanical barriers; such defenses include abundant lymphoid tissue, secretory IgA antibodies in respiratory secretions, and a rich vasculature that can rapidly deliver phagocytic leukocytes.

ETIOLOGY

Upper respiratory tract infections typically occur after insults to host defenses—such as allergic rhinitis, chemical irritation, trauma, and, especially, viral respiratory tract infections—that impair ciliary function and produce increased volumes of thin secretions and mucosal edema that block the narrow channels draining the sinuses and middle ear. Barotrauma, which results from a rapid change in atmospheric pressure, can intensify upper respiratory tract problems, particularly in patients with rhinitis, otitis, or sinusitis.

A Dutch case-controlled study of general practice patients with acute respiratory tract infections found that viruses accounted for 58% of cases; rhinovirus was the most common (24%), followed by influenza virus type A (11%) and corona viruses (7%). Group A streptococcus was responsible for 11%, and 3% of patients had mixed infections. Potential pathogens were detected in 30% of control patients who were free of acute respiratory symptoms; rhinovirus was the most common.2

Many upper respiratory tract infections are caused by viruses, and many of the bacterial infections in this area will resolve without antibiotic therapy.1 Unfortunately, antibiotics are overprescribed for upper respiratory tract infections; in the United States, antibiotics are prescribed for 50% to 75% of ambulatory patients seen for viral upper respiratory tract infections.3 Education programs can reduce inappropriate prescriptions.4 Because patient demand fuels antibiotic prescriptions for upper respiratory symptoms, another useful strategy is the delayed prescription, whereby the physician offers a prescription but suggests that it be filled only if symptoms fail to resolve without antibiotics. For immunocompetent patients who do not have high fevers or systemic symptoms, waiting periods have been proposed of 3 days for acute otitis media, 5 days for pharyngitis, and 10 days for lower respiratory symptoms.5 A waiting period of 7 to 10 days has been proposed for uncomplicated sinusitis.6

COMPLICATIONS

The complications of upper airway infections stem from several factors. The proximity of upper airway structures to the central nervous system and the presence of abundant vascular channels connecting the two account for some of the most severe complications. In addition, the numerous fascial planes of the head and neck provide potential spaces where infection can become sequestered. Furthermore, because the upper airway is narrow, infection in the neck may compromise the patency of the airway itself. Finally, immunosuppression renders persons vulnerable to unusual pathogens and unusual complications.

Sinusitis

Although infections of the paranasal sinuses are common, they are greatly overdiagnosed by patient and physician. Acute sinusitis is characterized by nasal congestion, purulent nasal discharge, fetid breath, facial pain that typically increases when the patient stoops forward, and, often, fever and other systemic symptoms. In most patients, acute sinusitis responds well to medical therapy; in a few persons, however, chronic sinusitis may result. Chronic sinusitis is characterized by purulent discharge, usually without fever, that persists for weeks or months.

ETIOLOGY

Viral, allergic, or vasomotor rhinitis is frequently an antecedent to sinusitis. Only 0.5% to 2% of nasopharnygitis cases lead to acute bacterial sinusitis7; nevertheless, in the United States, this complication develops in about 20 million persons each year.8 Nose blowing propels nasal fluid into the sinuses, potentially introducing viscid fluid and bacteria that can lead to sinusitis. Nasal polyps, deviation of the nasal septum, or hypertrophied adenoids may predispose to purulent sinusitis by obstructing sinus drainage. Cigarette smoke and overuse of topical decongestants impair ciliary action and alter the mucous blanket, predisposing to sinusitis. Contributing factors may include rapid changes in altitude, trauma, intranasal foreign bodies or tumors, cocaine abuse, and such systemic processes as cystic fibrosis and Kartagener syndrome (i.e., situs inversus, bronchiectasis, and sinusitis). Factors that predispose to chronic sinusitis include inadequately treated bacterial infections, long-term impairment of mucociliary clearance, obstruction of sinus drainage, and allergies and asthma.7

Nosocomial sinusitis occurs as a complication of nasotracheal intubation or, less often, the use of nasoenteric feeding tubes. Unexplained fever may be the presenting symptom, and computed tomography scanning is often required for diagnosis if the patient cannot localize the pain.

Immunosuppression increases the frequency and severity of sinusitis. Sinusitis is common in patients with AIDS and is often severe and refractory to treatment.

CLINICAL VARIANTS

The sinuses may be involved singly or, more often, in combination [see Figures 2a and 2b]. Frontal sinusitis and maxillary sinusitis are most common in adults; ethmoiditis is most common in children.

 

Figure 2. (a) The lateral wall of the right half of the nasal cavity: internal aspect. (b) The three nasal conchae have been partially removed.

Frontal sinusitis produces pain and tenderness over the lower forehead and purulent drainage from the middle meatus of the nasal turbinates. Maxillary sinusitis produces pain and tenderness over the cheeks. Pain is often referred to the teeth, and the hard palate may be edematous in severe cases. Purulent drain age is present in the middle meatus. Patients with ethmoidal sinusitis complain of retro-orbital pain and may have pain, tenderness, and even erythema over the upper lateral aspect of the nose. The anterior ethmoidal cells drain through the middle meatus, whereas the posterior cells drain through the superior meatus. Isolated sphenoid sinusitis, which occurs in only 3% of patients with sinusitis, is often misdiagnosed.7 This disorder has traditionally been considered to cause pain at the occiput or vertex; in fact, frontotemporal, retro-orbital, or facial pain is more common. Photophobia and tearing may be present. Purulent drainage is present in the superior meatus.

DIAGNOSIS

Clinical Features and Imaging Studies

Acute sinusitis

The diagnosis of acute sinusitis can usually be established on clinical grounds. Useful criteria are a poor response to decongestants; maxillary, facial, or tooth pain; and a duration of more than 7 days.9 Purulent nasal discharge is not specific for sinusitis and may occur in viral nasopharyngitis.10 The diagnosis of sinusitis can be confirmed by the finding of opacity when the frontal or maxillary sinuses are transilluminated or by radiographic findings such as mucosal thickening, sinus opacification, or air-fluid levels; sinus radiography has 90% sensitivity and 61% specificity for the diagnosis of acute sinusitis.7

Chronic sinusitis

The symptoms of chronic sinusitis are nasal congestion and discharge. Pain and headache are usually mild or absent, and fever is uncommon. Bone erosion may be present in chronic sinusitis. CT scans provide much more information than the traditional sinus x-ray series. Radiologic studies are essential in the diagnosis of severe, refractory, nosocomial, or complicated cases of sinusitis, but they are not necessary in routine cases.

Bacteriology

Because of technical difficulties in obtaining valid cultures, the bacteriology of sinusitis has been incompletely defined. Nasal cultures are unreliable because they correlate poorly with actual sinus fluid. Sinus punctures reveal that the most common pathogens in acute sinusitis are Haemophilus influenzae, pneumococci, streptococci, and Moraxella catarrhalis.9 Staphylococcus aureus has been isolated in nasal cultures from some patients with acute sinusitis, but the organisms are probably contaminants rather than the true causative agents. Nosocomial sinusitis is typically polymicrobial; S. aureus and gram-negative bacilli are often present.11

Chronic sinusitis is usually a polymicrobial infection. Anaerobic organisms have been isolated in as many as 51% of patients with chronic sinusitis; anaerobic streptococci and Prevotella species predominate.12 Anaerobes are also important in chronic sinusitis because they predominate in brain abscesses associated with sinus infections. S. aureus has been recovered from cultures in as many as 33% of patients with chronic sinusitis; enteric gram-negative bacilli may also be present.

Fungi such as Aspergillus, Mucor, and Rhizopus species produce invasive sinusitis in patients with leukemia or poorly controlled diabetes13,14and, occasionally, in normal hosts.12 Hypersensitivity reactions to airborne fungi contribute to some cases of chronic sinusitis.15 In immunocompromised patients, sinusitis may also be caused by Candida, Alternaria, Pseudomonas, Nocardia, Legionella, atypical mycobacteria, and certain parasites.16

DIFFERENTIAL DIAGNOSIS

Noninfectious processes must be considered in the differential diagnosis of sinusitis. Allergic or vasomotor rhinitis is by far the most common noninfectious cause of sinus symptoms. However, polyps, tumors, cysts, foreign bodies, and vasculitis (e.g., Wegener granulomatosis) occasionally produce symptoms of sinusitis.

TREATMENT

Medical Therapy

Acute sinusitis is treated with analgesics and topical heat for patient comfort. Decongestants are of paramount importance. Pseudoephedrine can be administered orally or by nasal spray. The danger of rebound after short-term use of nasal spray has probably been exaggerated. Patients should spray each nostril once and then wait 1 minute to allow the anterior nasal mucosa to shrink; a repeat spray will reach the upper and posterior mucosa, including the nasal turbinates and sinus ostia. This procedure can be repeated every 4 hours for several days, as needed. Antihistamines are not indicated, because they thicken secretions and impair drainage.9 Intranasal steroids are not necessary in most patients but may accelerate symptomatic improvements in some individuals17; however, steroids may be harmful. Nasal inhalation of warm, humidified vapor may relieve symptoms. Sleeping in a supine position or with the head of the bed elevated 45° promotes sinus drainage; patients with unilateral sinusitis should be encouraged to sleep with the unaffected side on the pillow. Other ancillary measures that may be helpful are nasal saline irrigations and aerobic exercise, which promotes mucous flow. Mucoregulating agents are often recommended, but this form of therapy has not been adequately studied.

Many patients with uncomplicated acute sinusitis respond well to decongestants and steam inhalations and do not need antibiotics.9,18,19Antibiotics should be used in moderately to seriously ill patients, in patients whose symptoms fail to respond to decongestants, and in patients who have complications. Older agents such as amoxicillin, doxycycline, and trimethoprim-sulfamethoxazole have produced good results [see Table 2].9 Second-line agents that are often prescribed include amoxicillin—clavulanate, cefuroxime, clarithromycin, azithromycin, and fluoroquinolones such as levofloxacin and helithromycin; they are no more effective than the less expensive first-line drugs.20,21 Because both H. influenzae and M. catarrhalis can produce β-lactamase, the use of antibiotics that resist these enzymes has attracted interest. However, antibiotics that are resistant to β-lactamase have not proved to be superior to those that are susceptible, possibly because comparative studies have been small and because many patients recover without antibiotic therapy. Much the same is true for penicillin-resistant pneumococci. Still, newer antibiotics that are active against these resistant organisms may be indicated in patients who have recently received antibiotics and in those who are seriously ill or fail to respond to older first-line antibiotics.7 The optimal duration of antimicrobial therapy is no more certain than are the indications for therapy or the choice of agents22; 7- to 14-day courses of antibiotics are traditional, but one trial found 3 days of trimethoprim-sulfamethoxazole to be as effective as 10 days of therapy.23 Clinical guidelines for the diagnosis and treatment of sinusitis are available from the American College of Physicians.24

Table 2 Antibiotic Therapy for Patients with Sinusitis

Drug

Dose

Cost/Mo ($)

Relative Efficacy

Comment

Amoxicillin

500 mg t.i.d. for 7–10 days

16

First-line therapy

May cause rash, hypersensitivity reaction, GI symptoms

Trimethoprimsulfamethoxazole

800 mg/160 mg b.i.d. for 3–10 days

18

First-line therapy

May cause rash, hematologic or GI symptoms

Doxycycline

100 mg b.i.d. for 7–10 days

92

First-line therapy

May cause photosensitivity, neutropenia

Surgical Therapy

Surgical intervention should be avoided in acute sinusitis unless the patient fails to respond to medical therapy and unless complications are present. Surgical drainage may be necessary in cases of chronic sinusitis or nosocomial sinusitis8; surgical drainage is mandatory in invasive fungal sinusitis.13,14

Functional endoscopic sinus surgery has provided an important advance in the surgical management of sinusitis. Patients with recurrent or chronic sinusitis who fail to respond to vigorous medical management may be candidates for this procedure. The patient should undergo a detailed preoperative evaluation, which usually includes a sinus CT scan. Surgery is performed using either local anesthesia with sedation or general anesthesia. A fiberoptic nasal endoscope is used to visualize the sinus ostia; when obstruction is present, it can be relieved by endoscopic aspiration. This technique restores patency and allows normal ciliary action to transport mucus to the natural ostium. Complications are uncommon when the procedure is performed by a skilled surgeon. Nasal endoscopy can also be used as an alternative to sinus puncture when it is necessary to obtain specimens for culture.25

COMPLICATIONS

The potentially life-threatening complications of sinusitis have become uncommon in the antibiotic era. However, frontal sinusitis can lead to osteomyelitis of the frontal bones, especially in children. Patients have headache, fever, and a characteristic doughy edema (i.e., Pott puffy tumor) over the affected bone. The organisms involved are those responsible for the underlying sinusitis, although S. aureus is more common in osteomyelitis than in sinusitis. Treatment should include decongestants for the sinusitis, high-dose intravenous antibiotics for the osteomyelitis, and surgical debridement when bone destruction is substantial. It is important to rule out coexisting brain abscess of the frontal lobe, which may be clinically occult.

Because the orbit is bordered on three sides by the paranasal sinuses, orbital infection can result from sinusitis. This disorder is most frequently a complication of ethmoidal sinusitis; it is caused by direct extension of infection through the lamina pap yracea. Orbital cellulitis usually begins with edema of the eyelids and rapidly progresses to ptosis, proptosis, chemosis, and diminished extraocular movements. Patients are usually febrile and acutely ill. Pressure on the optic nerve may lead to vision loss, which can be permanent; retrograde spread can lead to intracranial infection. Therapy with high-dose intravenous antibiotics is mandatory. Unless a specific pathogen can be isolated from the blood or purulent drainage, antibiotics should cover resistant organisms, including staphylococci and gram-negative rods. When an orbital abscess is present, surgical drainage may be necessary; CT and ultrasound studies aid this evaluation.

Retrograde spread along venous channels from the sinuses, the orbit, or the nose can produce septic cavernous sinus thrombophlebitis. Patients have high fever and appear toxic. Lid edema, proptosis, and chemosis are present. In cavernous sinus thrombophlebitis (but not in uncomplicated orbital cellulitis), third, fourth, and sixth cranial nerve palsies are prominent; the pupil may be fixed and dilated, and ophthalmoscopic examination may reveal venous engorgement and papilledema. Although at first the process is usually unilateral, spread across the anterior and posterior intercavernous sinuses makes it bilateral. Patients may exhibit alterations of consciousness, and lumbar puncture may reveal inflammatory changes in the cerebrospinal fluid. CT with a contrast agent or venography may help confirm the diagnosis. High-dose intravenous antibiotics, including antistaphylococcal drugs, are mandatory. Anticoagulants are not of established benefit and may even be harmful.

Sinusitis can lead to intracranial suppuration either by direct spread through bone or by spread through venous channels. Various syndromes, such as epidural abscess, subdural empyema, meningitis, and brain abscess, can result. Clinical findings, which vary greatly, range from the subtle personality changes associated with frontal lobe abscesses to headache, symptoms of elevated intracranial pressure, alterations of consciousness, visual symptoms, focal neurologic deficits, seizures, and, ultimately, coma and death. These are true medical emergencies requiring high-dose antibiotics and, except for meningitis, neurosurgical intervention [see 7:XXXVI Bacterial Infections of the Central Nervous System].

Otitis

ACUTE OTITIS MEDIA

Acute otitis media is one of the most common childhood infections; in the United States alone, the annual costs of the infection are estimated to be $3 billion to $5 billion.26 However, the incidence of otitis media declines with age, and it is uncommon in adults. Purulent otitis media results when bacteria ascend from the nasopharynx to the normally sterile middle ear. Abnormal eustachian tube function or obstruction caused by viral or allergic nasopharyngitis is considered important in the pathogenesis27; heredity may also play a role.

Etiology

The most common causes of purulent otitis media are the pneumococcus, nontypable strains of H. influenzae, and M. cartarrhalis28; the previously important group A streptococci are now uncommon but may be more aggressive than other pathogens.29,30 Other organisms that can cause acute otitis media are coagulase-negative staphylococci and anaerobic bacteria. Gram-negative bacilli and S. aureus can cause acute otitis media in neonates. Viruses and mycoplasmas are uncommon as the primary pathogens in acute otitis media, but in 41% of children with acute bacterial otitis, respiratory tract viruses are also present; respiratory syncytial virus is the most common causal organism, followed by parainfluenza and influenza viruses.31 Purulent nosocomial otitis is uncommon and occurs in only 4% of patients who have undergone endotracheal intubation; gram-negative bacilli are the responsible agents in this setting.31

Diagnosis

Pain and hearing loss are the classic presenting complaints of acute otitis media; fever is present in some cases, especially when pneumococci are responsible.29 The cornerstone of the clinical diagnosis is a bulging tympanic membrane, with impaired mobility and obscuration of the bony landmarks; these symptoms, coupled with a history of acute onset, suggest the diagnosis of acute otitis media.32Tympanic membrane perforation and otorrhea may occur. Concurrent conjunctivitis suggests the presence of H. influenzae.29

Needle aspiration of the middle ear can be used to confirm the diagnosis of purulent otitis media and to identify the causative organism; however, it is seldom necessary, because the bacteriology of otitis media is well defined and the clinical course is easy to monitor. Routine nose or throat cultures are not diagnostically reliable.

Differential Diagnosis

The major disorder considered in the differential diagnosis of acute otitis media is serous otitis media (also called otitis media with effusion). Fever and pain are absent in serous otitis media; although fluid is present in the middle ear, the tympanic membrane is usually retracted and the bony landmarks are preserved. The guidelines of the American Academy of Pediatrics and American Academy of Family Physicians (AAP/AAFP) recommend use of pneumatic otoscopy as the primary diagnostic method to distinguish acute otitis media from otitis media with effusion.33

Treatment

Acute otitis media may be treated with analgesics, decongestants, and antibiotics. If pain is present, evidence supports the use of analgesics; the management of pain, especially during the first 24 hours of an episode of acute otitis media, should be addressed regardless of the use of antibacterial agents.32 Although no treatment for otalgia has been well studied, the choices in analgesics include acetaminophen and ibuprofen for mild pain and narcotic analgesia with codeine for moderate or severe pain.32

In developed countries, nearly all affected patients are treated with antibiotics. In the United States, 20% of all prescriptions for oral antibiotics are issued for the treatment of otitis media; the average child consumes 3 months' worth of antibiotics in the first 2 years of life.34 As a result, H. influenzae, M. catarrhalis, and Streptococcus pneumoniae—the organisms most frequently responsible for acute otitis media—are manifesting dramatically increased resistance to antibiotics.

The utility of antibiotics in the treatment of acute otitis media is being reappraised.26,28,35,36 Their benefits appear to be modest; a meta-analysis concluded that to prevent one child from experiencing pain by 2 to 7 days after infection, 17 children must be treated with antibiotics.37 Further studies are required to determine which patients are most likely to benefit from antibiotics, which drugs are best, and how long therapy should be continued. A new approach that merits study is a delayed-therapy strategy, in which an antibiotic is prescribed when otitis media is diagnosed but the parents of the child are encouraged to fill the prescription only if the child's condition has not improved after 72 hours.38 The APA/AAFP guidelines consider observation with out use of antibiotics a therapeutic option in selected children with acute otitis media, depending on such factors as diagnostic certainty, uncomplicated illness, and assurance of follow-up.32

Most evidence regarding treatment of acute otitis media is derived from studies of children and adolescents. An evidence report of the Agency for Healthcare Research and Quality evaluated numerous studies to determine the effectiveness of antibiotics in preventing clinical failure in acute otitis media. In this report, clinical failure was defined as failure to resolve or improve clinical symptoms by a specific time interval. The meta-analysis reported that eight children with acute otitis media would need to be treated with ampicillin or amoxicillin (rather than receive no antibiotic treatment) to avoid one case failure.39

Numerous agents (e.g., amoxicillin, amoxicillin-clavulanate, ampicillin, trimethoprim-sulfamethoxazole, and the newer oral cephalosporins and macrolides) are clinically available for the treatment of acute otitis media [see Table 3]. If the decision is made to treat with an antibiotic, amoxicillin is recommended as first-line therapy for most patients because of the agent's general effectiveness, safety, and low cost.32 As in the case of sinusitis, drugs active against β-lactamase-producing bacteria have not proved to be superior to amoxicillin in the treatment of acute otitis media, perhaps because antibiotics are only slightly more effective than placebo40; 81% of patients with acute otitis media recover without any antibiotic therapy.41 Although antibiotics are generally administered for 10 days, 5 days of treatment may be equally effective in uncomplicated cases.42,43 A single intramuscular dose of ceftriaxone is also as efficacious as 10 days of oral therapy.44 Myringotomy does not hasten recovery but is indicated for patients with intractable pain, progressive deafness, or early mastoiditis or for those who respond poorly to medical therapy.

Table 3 Antibiotic Therapy for Children with Acute Otitis Media*

Drug

Dose

Comment

Amoxicillin

80–90 mg/kg/day for 7–10 days

First-line therapy

Cefdinir

7 mg/kg twice daily for 7–10 days

For patients with non-type 1 reactions to penicillin

Cefpodoxime

10 mg/kg/day once daily for 7–10 days

For patients with non-type 1 reactions to penicillin

Cefuroxime

30 mg/kg/day in two divided doses for 7–10 days

For patients with non-type 1 reactions to penicillin

Azithromycin

10 mg/kg/day on day 1, followed by 5 mg/kg/day for 4 days

For patients with type 1 reactions to penicillin

Clarithromycin

15 mg/kg/day in two divided doses for 7–10 days

For patients with type 1 reactions to penicillin

Trimethoprim-sulfamethoxazole

6–10 mg/kg/day t.i.d. or q.i.d. for 7–10 days

For patients with type 1 reactions to penicillin; should be used with caution because of high incidence of resistant pneumococci

*For information regarding side effects, cross-reactivity and complications of specific agents, see7:XIV Antimicrobial Therapy.

Complications

The prognosis for acute otitis media is excellent. Chronic serous otitis media, hearing loss, and recurrent purulent otitis media are the most common complications. Recurrences are usually caused by reinfection rather than relapse or persistent infection; antibiotics may be used for chemoprophylaxis of recurrent otitis in children.28 Tympanostomy tubes may be helpful in children with numerous recurrences.

Acute mastoiditis, which is now rare, develops in patients with inadequately treated otitis media. Presenting symptoms consist of fever, otalgia, and postauricular edema and tenderness. The tympanic membrane is abnormal in all cases; perforations and otorrhea are present in about half of cases. Mastoid x-rays are usually abnormal. The species of bacteria responsible for mastoiditis are the same as those that cause acute otitis media. Patients who fail to respond to antibiotic therapy within 48 hours and those with CNS complications should be considered for early mastoidectomy.

Other rare suppurative complications of acute otitis media include purulent labyrinthitis, meningitis, lateral sinus thrombosis, and brain abscess. Bacteremia can be documented in 3% of young febrile children with otitis media, but it does not appear to alter the prognosis or to warrant parenteral antibiotic therapy.32

CHRONIC OTITIS MEDIA

Chronic otitis media, which can occur at any age, results from neglected or recurrent acute otitis media. Pain and fever are usually absent but can occur during sporadic flare-ups.45 Diminished hearing and foul otorrhea are major symptoms.

Physical examination discloses perforation of the tympanic membrane. Central perforations of the pars tensa are associated with benign disease, but peripheral perforations may occur with invasive cholesteatomas. X-rays reveal sclerosis of the mastoid air cells and bone destruction. Various organisms can be cultured from middle-ear drainage, including P. aeruginosa, staphylococci, streptococci, and enteric gram-negative bacilli. Anaerobes are present in 16% of cases, almost always in mixed infections with aerobes. Systemic antibiotics are generally of little benefit, but antibiotic eardrops may be helpful; quinolones appear to be more effective and safer than aminoglycosides.46Surgery is required in advanced cases. Without therapy, chronic otitis media can cause the same intracranial suppurative complications seen in acute otitis media.

OTITIS EXTERNA

Otitis externa is a common, generally benign inflammatory disorder that is usually precipitated by excessive moisture in or trauma to the external auditory canal. Patients have pruritus or pain, or both, that may be severe. Crusting, inflammation, and discharge in the canal are typical findings. Pain resulting from movement of the external ear helps distinguish otitis externa from otitis media. A broad range of organisms, including gram-positive cocci, gram-negative bacilli, and fungi, can cause otitis externa. Excellent results are produced by topical therapy with eardrops containing polymyxin B, neomycin, and corticosteroids or eardrops containing acetic acid and corticosteroids.47 Patients occasionally acquire true cellulitis of the external ear; such patients require systemic 2antibiotics and even debridement of infected cartilage.

Malignant otitis externa, an infection with P. aeruginosa that progressively invades the cartilage, soft tissue, and skull, is a rare condition that occurs in diabetic patients. Neurologic complications can be lethal. Prolonged, maximal parenteral therapy with combinations of antipseudomonal agents, such as tobramycin and piperacillin, is generally recommended. Mono therapy with intravenous ceftazidime and prolonged therapy with oral cipro floxacin have been successful. Other antibiotics that may prove useful alone or in combination are aztreonam, cefepime, imipenem, and meropenem. Aggressive surgical debridement has been a mainstay of treatment; however, it may be required less often in patients who are treated early and aggressively with antibiotics. CT scans are superior to magnetic resonance imaging for early diagnosis, but either technique can be used to monitor patients for bone destruction and neurologic complications; should these sequelae occur, debridement is required. Mortality is high but has decreased since 1990 because of the introduction of new drugs and a growing emphasis on aggressive diagnosis and treatment. Aspergillus is a rare cause of malignant otitis externa.

Pharyngitis

Although pharyngitis is one of the most common problems in clinical practice, a surprising number of practical questions remain unanswered.48 Group A streptococci are the most therapeutically important cause of pharyngitis, although in terms of frequency, they cause as few as 5% of the cases of pharyngitis and as many as 38% of the cases of tonsillitis.49

STREPTOCOCCAL PHARYNGITIS

Diagnosis

Four clinical criteria have been proposed as suggestive of group A streptococcal pharyngitis: tonsillar exudates, tender anterior adenopathy, absence of cough, and history of fever. Unfortunately, however, there is considerable overlap between streptococcal and viral pharyngitis.

Because streptococcal and viral pharyngitis cannot be distinguished reliably on clinical grounds,49 laboratory studies are necessary to make a diagnosis of streptococcal pharyngitis. Throat cultures remain the standard method for identifying group A streptococci in the pharynx. In addition, rapid diagnostic tests suitable for office use are available. These procedures entail the extraction of streptococcal antigens from throat swabs and the rapid identification of the antigens through immunologic tests such as latex agglutination or enzyme-linked immunosorbent assay (ELISA). The sensitivity of these tests ranges from 77% to 95%; specificity ranges from 86% to 100%. Thus, these tests are acceptable for clinical practice; the Infectious Diseases Society of America no longer recommends throat cultures to confirm the results of rapid antigen tests.50,51

The diagnosis of streptococcal pharyngitis is suspected on clinical and epidemiologic grounds and confirmed by a rapid antigen test or throat culture. Although the laboratory recognition of group A streptococci is straightforward [see 7:I Infections Due to Gram-Positive Cocci], it is difficult to determine whether the organisms are responsible for a patient's symptoms. The carrier rate of group A streptococci in healthy persons approaches 20%, and even in patients with symptomatic pharyngitis, only 50% of those patients with positive throat cultures demonstrate a serologic response to streptococci. Except for a serologic determination, there is no proven method for distinguishing between the carrier state and active infection. Similarly, controversy exists about the need for obtaining cultures from asymptomatic family contacts of patients with streptococcal pharyngitis, for treating asymptomatic persons with small numbers of group A streptococci in their throat cultures, and for performing follow-up cultures after therapy. On balance, all of these procedures are probably unnecessary unless the patient is highly susceptible to rheumatic carditis because of previous acute rheumatic fever.51,52

Treatment

Fortunately, no uncertainty exists about the therapy for streptococcal pharyngitis in symptomatic patients. The disease is ordinarily self-limited, but early antibiotic therapy can alleviate symptoms,53 as can simple analgesic antipyretics. However, the extent of symptomatic relief appears to be minimal. A meta-analysis found that antibiotics shorten the duration of symptoms by a mean of 1 day about halfway through the illness (the time of maximal effect) and by about 16 hours overall.54 Evidence from the meta-analysis also suggests that protecting sore throat sufferers against suppurative and nonsuppurative complications can be achieved only by giving antibiotics to many patients who will derive no benefit from them.54 Antibiotics also limit droplet spread and prevent rheumatic fever. Because rheumatic fever is now rare in the United States and can be prevented even when therapy is delayed as long as 9 days after the onset of symptoms, treatment need not be started until rapid-antigen assay or throat culture results are available.55

The goal of antibiotic therapy is the eradication of group A streptococci from the nasopharynx. In more than 80% of patients, this result can be achieved with oral penicillin V, 250 mg four times a day for 10 days [see Table 4]. Twice-a-day dosing is also effective in children and may improve compliance.56 When patient compliance is in doubt, a single injection of 600,000 to 1.2 million units of benzathine penicillin G will be at least as effective. In patients who are allergic to penicillin, oral erythromycin or one of the newer macrolides (i.e., clarithromycin or azithromycin) is an excellent alternative, but it must be continued for 10 days. Tonsillectomy was once widely performed on children to prevent recurrent pharyngitis, but it has largely been abandoned.

Table 4 Antibiotic Treatment for Streptococcal Pharyngitis*

Drug

Dose

Cost/Mo ($)

Relative Efficacy

Comment

Benzathine penicillin G

1.2 million units (600,000 for patients < 60 lb) I.M.

First choice when compliance is critical

Penicillin V

250 mg q.i.d. (250 mg b.i.d. for children) p.o. for 10 days

21

First choice for oral therapy

Cephalexin

500 mg b.i.d., p.o. (25–50 mg/kg/day t.id. or q.i.d., p.o., for children > 1 yr)

207

For patients with non-type 1 reactions to penicillin

Erythromycin estolate

30–50 mg/kg/day p.o. in two to four divided doses (maximum, 2 g/day)

34

For patients with type 1 reactions to penicillin

May cause GI side effects

Clarithromycin

250 mg b.i.d., p.o. for 10 days (15 mg/kg/day in two divided doses for 7–10 days for children ≥ 6 mo)

220

For patients with type 1 reactions to penicillin

Causes fewer GI side effects than erythromycin

Azithromycin

500 mg p.o. on day 1, followed by 250 mg/day in a single dose for 4 days (12 mg/kg/day p.o. once daily for 5 days, for children ≥ 2 yr; maximum, 500 mg/day)

239

For patients with type 1 reactions to penicillin

Causes fewer GI side effects than erythromycin

*For information regarding side effects, cross-reactivity, and complications of specific agents, see7:XIV Antimicrobial Therapy.

Although only a minority of sore throats are caused by group A streptococci, 73% of adults who consult physicians for pharyngitis receive antibiotics; 68% of these prescriptions are for nonrecommended agents.57 Azithromycin in 3-day regimens58 and cephalosporin in 5- to 10-day regimens are effective,59,60 but these drugs are expensive and the regimens are not currently recommended in the United States.48

OTHER FORMS OF BACTERIAL PHARYNGITIS

Other bacterial causes of pharyngitis are uncommon. Groups C and G streptococci can cause pharyngitis, but complications are rare. Gonococci transmitted by oral sex can produce sore throat, erythema, exudates, and lymphadenopathy; asymptomatic colonization of the pharynx may occur. Meningococci sometimes cause symptomatic pharyngitis but are more commonly found in throat cultures of asymptomatic persons. H. influenzae pharyngitis can be extremely painful but is rare in adults; epiglottitis is a life-threatening complication of this type of pharyngitis. In patients who have not been immunized, Corynebacterium diphtheriae can cause painful membranous pharyngitis, often characterized by dysphagia and prominent edema of the neck. Arcanobacterium haemolyticum, formerly known asCorynebacterium haemolyticum, can cause pharyngitis and scarlatiniform rash, particularly in teenagers and young adults; administration of penicillin or erythromycin produces rapid relief of symptoms. Yersinia enterocolitica is an uncommon cause of pharyngitis; the pharyngitis may be present without enteritis, particularly in adults.

Many other bacterial species can be cultured from the pharynges of both symptomatic and asymptomatic patients [see Table 1], but they almost never cause pharyngitis. In particular, although pneumococci and staphylococci commonly reside in the nasopharynx and can cause severe disease in other parts of the respiratory tract, they do not cause pharyngitis. Mycoplasma pneumoniae causes pharyngitis in children and adults, but this diagnosis is seldom made in the absence of pneumonitis. Chlamydophila pneumoniae (formerly Chlamydia pneumoniae) can also cause pharyngitis, which may be protracted.61

Treponema pallidum, a spirochete that is not part of the normal flora, can cause pharyngitis in patients with primary or secondary syphilis. Among the other causes of pharyngitis, Mycobacterium tuberculosis is very rare. Candida albicans, which is part of the normal mouth flora, can produce painful oropharyngeal moniliasis, or thrush, if antibiotics or debilitating illnesses (particularly HIV infection) upset microbial interactions and host defenses. This disease is characterized by a white, cheesy exudate that can be scraped off to demonstrate yeast forms by smear and culture. Nystatin oral suspension is therapeutically effective, but frequent, large doses may be required. Clotrimazole troches are also effective. Patients with HIV infection may require systemic therapy with fluconazole. Other forms of fungal pharyngitis are rare.

Deep Tissue Infections

Infections originating in the pharynx may extend by contiguous spread to the deep tissues of the pharynx and neck. In the neck, numerous fascial planes create a variety of potential spaces where infection can become loculated to form a phlegmon or a full-fledged abscess. Although these processes are now uncommon, prompt recognition is mandatory because antibiotics and surgical drainage are required to control infection and to prevent obstruction of the airway, invasion of vital neurologic and vascular structures, and spread of infection to the mediastinum and bloodstream.

PERITONSILLAR ABSCESS

Peritonsillar abscess, also called quinsy throat, is a complication of streptococcal tonsillitis most often seen in adolescents and young adults. Group A streptococci are the primary cause of the condition, although most peritonsillar abscesses also harbor mixed oral bacteria, with a predominance of anaerobes.

Patients have fever and sore throat, often with pain referred to the ear. Dysphagia prevents the patient from swallowing saliva, commonly causing drooling; edema and pain produce a characteristic muffled, so-called hot-potato voice. The affected tonsil is visibly displaced forward, downward, and toward the midline; the soft palate may be edematous. Trismus occurs in some patients. CT scans are important in diagnosis and management.

Treatment consists of parenteral penicillin and surgery. The traditional approach consists of immediate incision and drainage, followed by tonsillectomy 4 to 6 weeks later; early tonsillectomy has also produced excellent results. Treatment with needle aspiration and oral antibiotics has also been successful; 80% to 92% of patients with peritonsillar abscess can be cured with this approach, thereby obviating hospitalization and surgery.62

RETROPHARYNGEAL AND PARAPHARYNGEAL INFECTIONS

Retropharyngeal infections are most common in childhood because the lymph nodes in this region atrophy during adult life. Patients have fever and systemic toxicity, as well as neck pain, dysphagia, muffled voice, and respiratory stridor. Physical findings include erythema and bulging of the posterior wall of the pharynx. CT scans and lateral-view x-rays of the neck are extremely useful, invariably demonstrating soft tissue swelling and forward displacement of the larynx [see Figures 3a, 3b, and 3c]. Although the bacterial agent of retropharyngeal infections is not determined in many patients, streptococci and other mouth flora predominate. Penicillin is the traditional antibiotic of choice, but agents that provide a broader spectrum of antibacterial coverage may be justified until culture data are available. Surgical drain age is vital to prevent asphyxiation and extension of infection to the mediastinum. Infections of the retropharyngeal space must be distinguished from infections of the prevertebral space.

 

Figure 3. (a) An oblique-view x-ray of the skull of a 16-year-old boy with fever, headache, and doughy edema of the forehead shows soft tissue swelling and a small area of underlying cortical irregularity indicative of osteomyelitis. (b) Sinus film reveals severe pansinusitis. (c) Because of subtle personality changes, a CT scan was taken; it revealed a large frontal lobe abscess. At surgery, 45 ml of pus was evacuated. Anaerobic streptococci were isolated from the subperiosteal collection and the brain abscess. Prolonged penicillin therapy and surgical management led to recovery.

The prevertebral space lies posterior to the retropharyngeal space and is separated from it by the prevertebral fascia. Infection of the prevertebral space often originates from osteomyelitis of the cervical vertebrae. This infection is frequently caused by staphylococci and may lead to spinal cord damage unless treated through an approach that combines immobilization, antistaphylococcal antibiotics, and external drainage.

The parapharyngeal space is demarcated by the parotid gland and the internal pterygoid muscle laterally and by the superior constrictor muscle medially. The internal jugular vein, carotid artery, and cranial nerves IX, X, and XII pass through the parapharyngeal space. Infection can reach the parapharyngeal space from the pharynx or from parotid or dental foci. Patients have severe trismus, externally visible inflammation behind the angle of the jaw, and inflammation in the lateral wall of the pharynx, with medial displacement of the tonsil. Treatment consists of intravenous penicillin and drainage; CT-guided needle aspiration may be effective in some patients, but surgical drainage from behind the angle of the jaw is required in others.

Infections of the parapharyngeal space occasionally spread to the jugular vein and cause the syndrome of postanginal sepsis (Lemierre syndrome), which is characterized by the presence of septic phlebitis, septic pulmonary emboli, and anaerobic bactere mia. Pharyngitis and dental infections may also lead to postanginal sepsis. Facial swelling is an early diagnostic clue to this syndrome. CT is important for detecting abscesses, and ultrasonography is helpful for identifying jugular vein thrombosis. Anaerobic gram-negative bacilli, such asFusobacterium species, are typically responsible for the condition. Management requires intravenous administration of penicillin; metronidazole and clindamycin are useful alternatives. Heparin, venous ligation, and surgical thrombectomy have also been advocated, but data do not allow firm guidelines to be established for these interventions.

LUDWIG ANGINA

Ludwig angina is a cellulitis of the submandibular, sublingual, and submental regions. In many patients, the infection originates from a dental focus. Clinical features include fever, marked toxicity, and a rapidly progressive brawny edema in the floor of the mouth and the anterior neck. Elevation of the tongue impedes swallowing, and airway obstruction may be lethal. Streptococci and mouth flora are the most common etiologic agents, but H. influenzae, staphylococci, and gram-negative bacilli have also been implicated; broad antibiotic coverage may be necessary initially. Because endotracheal intubation can provoke laryngeal spasm, tracheostomy may be necessary to preserve the airway. Surgical decompression may be required.

Acute Epiglottitis (Supraglottitis)

No infection of the upper respiratory tract is more rapidly progressive or more lethal than acute epiglottitis, also known as supraglottitis. Acute epiglottitis occurs most commonly in children between 2 and 8 years of age and is more frequent in boys. The incidence of epiglottitis in childhood is declining rapidly in populations that have received H. influenzae type b vaccinations. Cases in adults appear to be increasing, however, perhaps because of improved diagnosis.

ETIOLOGY

The major cause of acute epiglottitis in children and adults is H. influenzae type b. Other pathogens, including pneumococci, streptococci, staphylococci, and Klebsiella pneumoniae, can produce an identical syndrome. Although viral epiglottitis is rare, this syndrome can occur secondary to infection with herpes simplex virus type 1.63 In the immunocompromised host, additional organisms may be responsible, including Candida and Kingella kingae; fortunately, such cases are rare.

DIAGNOSIS

Epiglottitis begins with startling rapidity; severe sore throat and fever progress rapidly to dysphagia, with retention of secretions and drooling. Systemic toxicity is marked; if the illness is not treated, dyspnea and progressive respiratory obstruction occur in a matter of hours.

Although uncommon, acute epiglottitis in adults often extends to the supraglottic structures, and edema may be more prominent than acute inflammation. Whereas children with acute epiglottitis usually present with respiratory distress, adults may first complain of pharyngeal symptoms (severe pain and odynophagia) before developing respiratory symptoms.64 The course of the disease in adults is slower than it is in children, often extending over several days because of the larger diameter of the adult airway.

Acute epiglottitis is a medical emergency. The key to the diagnosis is a swollen, edematous, cherry-red epiglottis. Simple inspection of the pharynx is usually unrewarding. Furthermore, any instrumentation, even a tongue blade, can provoke spasm and total airway obstruction, although adults are at lower risk for this complication. Therefore, unless acute respiratory distress is present, a lateral-view x-ray of the neck should be taken immediately. If the film does not demonstrate epiglottal edema, indirect laryngoscopy can be undertaken; if edema is present, however, the diagnosis is confirmed, and instrumentation is unnecessary. In all cases, patients must be monitored continuously for signs of respiratory obstruction.

DIFFERENTIAL DIAGNOSIS

In the differential diagnosis in children, it is important to distinguish between epiglottitis and croup caused by viral laryngitis with laryngeal and subglottal edema and airway obstruction. Croup usually affects younger patients and progresses more slowly than epiglottitis, and patients with croup present with hoarseness and a characteristic cough. In addition, in croup, the epiglottis is normal or only minimally inflamed on physical or radiographic examination. Cold, humidified oxygen is the mainstay of treatment of croup, and close observation is vital because emergency intubation or tracheostomy may be necessary. In children, bacterial tracheitis or membranous croup may present as severe laryngotracheitis, requiring antibiotic therapy and respiratory support. In patients of all ages, angioneurotic edema of the larynx, foreign bodies lodged in the upper airway, or impingement on the airway by various mass lesions may initially be confused with epiglottitis, but these conditions should be readily recognizable on physical examination and radiography.

TREATMENT

Although tracheostomy is the traditional means of securing a patent airway in patients with epiglottitis, nasotracheal intubation is safe and effective. As a result, direct laryngoscopy by an experienced observer who is prepared to proceed with intubation (or, if necessary, tracheostomy) can be relied on for diagnosis when taking x-rays would produce excessive delay.

Because there is no margin for error, initial therapy with high-dose intravenous antibiotics effective against H. influenzae (including penicillinase-producing strains), other gram-negative bacilli, and staphylococci is warranted. Many regimens are available, including cefuroxime or cefamandole, ampicillin-sulbactam, meropenem, imipenem-cilastatin, and a third-generation cephalosporin combined with a penicillinase-resistant penicillin. The choice of drugs depends on the results of throat and blood cultures and on ampicillin-sensitivity testing of H. influenzae isolates. A mist tent may be helpful. Steroids are sometimes advocated to reduce the edema, but their effectiveness has not been tested in controlled clinical trials. Above all, preservation of the airway is critical; nasotracheal intubation or tracheostomy is required in about half of all cases. If the airway can be protected while antibiotics take effect, most patients can be saved.

Miscellaneous Upper Respiratory Tract Infections

Many other infectious processes can invade the upper respiratory tract and adjacent regions of the head and neck. Common viral infections of the oropharynx are primary herpes simplex gingivostomatitis and adenovirus and coxsackievirus infections. Spirochetes play a role in ulcerative gingivitis and periodontitis. Actinomyces israelii can produce chronic burrowing infections of the gums and jaw, occasionally with secondary involvement of the respiratory tract. Although rare in the United States, rhinoscleroma, believed to be caused by Klebsiella rhinoscleromatis, can occur in immigrants from developing countries or in HIV-infected persons. S. aureus may produce acute bacterial sialadenitis or suppurative parotitis; less commonly, gram-negative bacilli or even anaerobes produce parotitis in hospitalized patients.

Many bacterial species have been implicated in a variety of dental infections. Mixed infections with normal mouth flora can occur in debilitated patients. Fusobacteria and spirochetes can cause gingivitis (trench mouth) or necrotic tonsillar ulcers (Vincent angina); patients have foul breath, pain, and dirty-gray membranous inflammation that bleeds easily. Oral irrigations and penicillin are effective therapy. A similar combination of spirochetes and other bacteria can produce cancrum oris, a rare but extremely serious invasive gangrene of the mouth that occurs only in malnourished infants or in patients with advanced malignant disease or immunosuppression. Anaerobes may play a role in chronic or recurrent tonsillitis.41 Dental infection is the leading cause of necrotizing cervical fasciitis.

Many noninfectious processes in these regions can produce symptoms that mimic bacterial infection. Aphthous stomatitis may be the most common example. Drug reactions and primary dermatologic diseases cause oral and pharyngeal ulcerations. Vasculitis, carcinomas, lymphomas, and sarcoidosis of the upper airway can also mimic bacterial infection. Even subacute thyroiditis, which may produce fever and referred pain, may be mistaken for pharyngitis or otitis.

Acknowledgment

Figures 1 and 2 Tom Moore.

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Editors: Dale, David C.; Federman, Daniel D.