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BACTERIAL INFECTIONS OF THE UPPER RESPIRATORY TRACT

Author(s)

HARVEY B. SIMON M.D., F.A.C.P.

July 2003

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Overview of Upper Respiratory Tract Infections

Upper respiratory tract infections range from common, benign processes, such as nasopharyngitis, to uncommon, potentially lethal processes, such as epiglottitis. Pathogens range from pyogenic bacteria [see 15: Infections Due to Gram-Positive Cocci and 23: Infections Due to Mycobacteria] to Chlamydia [see 28: Diseases Due to Chlamydia], mycoplasmas [see 27: Infections Due to Mycoplasmas], respiratory viruses [see 31: Respiratory Viral Infections], and, on occasion, fungi [see 37: 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 varied 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 the patient.

Many host defense mechanisms protect the upper airway from infection. Mechanical defenses tend to prevent penetration by 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.

Many upper respiratory tract infections are caused by viruses, and many of the bacterial infections in this region will resolve without antibiotic therapy.1 Unfortunately, antibiotics are overprescribed for upper respiratory tract infections. In 1998, for example, at least 55% of the 41 million antibiotic prescriptions given to ambulatory patients in the United States were inappropriate.2

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. Nose blowing propels nasal fluid into the sinuses, potentially introducing viscid fluid and bacteria that can lead to sinusitis.3 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 (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.

Nosocomial sinusitis occurs as a complication of nasotracheal intubation or, less often, the use of nasoenteric feeding tubes.4 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 Figure 2a and 2b]. Frontal sinusitis and maxillary sinusitis are most common in adults; ethmoiditis is most common in children.

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 drainage 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. 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.5 Purulent nasal discharge is not specific for sinusitis and may occur in viral nasopharyngitis.6 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.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 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.5,7 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.8

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.9 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.

Viruses seldom cause clinical sinusitis. Such fungi as Aspergillus, Mucor, and Rhizopus species produce invasive sinusitis in patients with leukemia or poorly controlled diabetes10,11 and, occasionally, in normal hosts.10 In immunocompromised patients, sinusitis may also be caused by Candida, Alternaria, Pseudomonas, Nocardia, Legionella, atypical mycobacteria, and certain parasites.12

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 (such as Wegener granulomatosis) occasionally produce symptoms of sinusitis.

TREATMENT

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 a 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 when needed. Antihistamines are not indicated, because they thicken secretions and impair drainage.5 Intranasal steroids are not necessary in most patients but may accelerate symptomatic improvements in some individuals13; they may be harmful. Nasal inhalation of warm, humidified vapor may relieve symptoms. Sleeping supine 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 have not been adequately studied.

Many patients with uncomplicated acute sinusitis respond well to decongestants and steam inhalations and do not need antibiotics.5,14 Antibiotics 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.5 Second-line agents that are often prescribed include amoxicillin-clavulanic acid, cefuroxime, clarithromycin, azithromycin, and levofloxacin; they are no more effective than the less expensive first-line drugs.15,16 Because both H. influenzae and M. catarrhalis can produce ß-lac-tamase, the use of antibiotics that resist these enzymes has attracted interest. However, antibiotics that are resistant to ß-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. The optimal duration of antimicrobial therapy is no more certain than are the indications for therapy or the choice of agents; 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.17 Clinical guidelines for the diagnosis and treatment of sinusitis are available.18

Surgical intervention should be avoided in acute sinusitis unless the patient fails to respond to medical therapy and complications are present. Surgical drainage may be necessary in cases of chronic sinusitis or nosocomial sinusitis8 and is mandatory in invasive fungal sinusitis.10,11

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. 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.19

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