Communicable Diseases Update
Acute Community-Acquired Sinusitis

Jeffrey Lauer, M.D.
Jeffrey Lauer, M.D. is a Clinical Instructor in Medicine, Division of Infectious and
Communicable Diseases, Department of Medicine, University of Florida
and Duval County Health Department.

The paranasal sinuses are aerated cavities in the bones of the face that develop as outpouches of the nasal cavity and communicate with this cavity throughout life. The maxillary and ethmoid sinuses are present at birth; the frontal and sphenoid sinuses develop after ages 2 and 7, respectively.¹ The sinuses reduce overall skull weight, participate in warming and humidification of inspired air, and add resonance to the voice. The sinuses are lined with ciliated pseudostratified epithelium containing mucus-producing goblet cells, similar to the nasal cavity but with less density.² The ciliated cell beating carries mucus and contaminants out of the sinuses toward the sinus openings (ostia) at a speed of up to 1 cm/min..³ The mucus blanket changes two to three times each hour. Obstruction of the ostia and/or delay in mucociliary transport lead to accumulation of secretions and subsequently to the development of sinusitis. The paranasal sinuses are normally sterile unlike the nasal passages. The mechanisms maintaining this sterility include the mucociliary clearance system, the immune system, and possible nitric oxide production within the sinus cavity. ⁴

The classification of sinusitis can be based on a number of parameters: 1) patient's immune status, 2) etiologic pathogen (viral, bacterial, fungal), and 3) the duration of sinusitis (acute, subacute, chronic, recurrent). Acute sinusitis is defined as sinusitis lasting 4 weeks or less, while subacute when symptoms persist for 4 to 12 weeks and chronic when symptoms last longer than 12 weeks. During the first 7 to 10 days of illness it may be difficult to classify the etiology of sinus symptoms as either from a viral or bacterial cause and decide if antimicrobials are indicated. The appropriate classification is important so that treatment outcomes can be evaluated and the correct treatment defined and instituted. This paper will focus on acute community-acquired bacterial sinusitis highlighting only those areas of the other types of sinusitis to demonstrate relationships, similarities and differences.

The most commonly involved sinus with any type of sinusitis is maxillary; followed in frequency by ethmoid, frontal, and sphenoid. A viral infection of the upper respiratory tract is the most common precursor to bacterial sinusitis and has lead to the use of the term and definition of viral rhinosinusitis (VRS). VRS is defined as an initial viral syndrome resulting in thickening of sinus mucosa, possible obstruction of the ostia, and the signs and symptoms of classic sinusitis with or without rhinitis. It is unclear if the presence of the virus in the sinus is needed for the sinus symptoms or if symptoms result solely from the associated inflammatory response. The VRS usually resolves within 7-10 days without specific therapy. Two new antiviral agents, Pleconaril and AG7088 are currently being evaluated as therapies for VRS caused by rhinoviruses or enteroviruses. It is hoped that these will one day be effective in shortening the clinical course of VRS. It is estimated that 0.5 to 2 percent of VRS infections are complicated by clinically evident acute bacterial sinusitis. In the United States, the incidence of VRS in adults is estimated to be 2 to 3 episodes per year and in children double that amount. Using the U.S. population and an average 4 VRS episodes per year, then an estimated 1 billion cases of VRS occur annually with an expected progression to acute bacterial sinusitis in 20 million patients. The 1991 data from the National Ambulatory Medical Care Survey indicated 11.57 million physician-patient contacts for acute upper respiratory illness and 2 million visits per year for presumed acute bacterial sinusitis. Thus it would appear that one in one hundred VRS patients and one in ten acute sinusitis patients seek physician care for their illness. This has tremendous associated social and economic impact.

VRS and its complication of acute bacterial sinusitis have seasonal patterns of occurrence based on the virus involved. Early fall and late spring the rhinovirus has the highest incidence, while in winter and early spring the likely agents are coronavirus, respiratory syncytial virus and influenza. Acute community-acquired sinusitis can result from other causes as well (e.g. swimming, allergies, nasal obstruction secondary to polyps, tumor or foreign bodies), and these demonstrate no particular seasonal pattern. Also, those individuals with defects in immunity (HIV, agammaglobulinemai), delayed or absent mucociliary activity (Karagener's, cystic fibrosis), structural defects (cleft palate), and WBC functional abnormalities (chronic granulomatous disease, Wegerner's granulomatosis) are at risk for the development of acute sinusitis that may occur regularly or develop into chronic sinus disease. Dental infections may cause 5-10% of all cases of maxillary sinusitis; the roots of the upper back teeth (second bicuspid, first and second molars) abut the floor of the maxillary sinus.

The pathogenesis of VRS and acute community-acquired bacterial sinusitis is still debated. The most widely investigated viral pathogen is the rhinovirus. It has a unique ability to evade the host defenses in the upper respiratory tract and in non-immune volunteers has a >90% infection rate after intranasal innoculation.⁵ After deposition in the nose there is presumed transport to the posterior pharynx and attachment to rhinovirus receptor ICAM-1 (intercellular adhesion molecule-1).⁶ It is the resultant inflammatory and parasympathic responses, rather than any direct cytotoxic effect of the virus, that cause the classic symptoms of the cold and the physical changes noted in the sinuses. Sinus cavity abnormalities were seen in 87% of patients with colds and could involve any of the paranasal sinuses (Table 1).

The inflammatory process results in increased mucosal edema, increased mucus production, and delayed or absent mucociliary clearance with eventual ostial obstruction. Without adequate physiologic sinus drainage, bacteria that normally colonize the nasal passages or the pharynx can be deposited into the sinuses when sneezing, coughing or blowing the nose. This process is believed to account for the development of acute community-acquired bacterial sinusitis following an upper respiratory tract viral illness.

Manifestation

Symptoms of VRS and acute bacterial sinusitis can include purulent nasal or postnasal drainage, nasal congestion, and sinus pain or pressure. The location of the sinus pain or pressure depends on the sinus involved. Maxillary sinus pain is often perceived as being located in the cheek or upper teeth; ethmoid sinus pain, between the eyes or retroorbital; frontal sinus pain, above the eyebrow; and sphenoid sinus pain, in the upper half of the face or retroorbital with radiation to the occiput. Sinus pain is frequently worse when the patient bends forward or is supine. These symptoms, although suggestive of sinus involvement, does not identify the cause and if early in the course may represent a viral etiology. The persistence of cold symptoms for greater than 7 to 10 days (or longer than usual for a particular patient) is the most consistent clinical feature of acute bacterial sinusitis. Complete opacification of the maxillary or frontal sinus, shown by transillumination with a strong flashlight, constitutes good evidence of sinusitis. But the differentiation of viral from bacterial or a combination of viral-bacterial can be difficult. There is limited sensitivity and specificity for many of the clinical findings routinely used to evaluate for sinusitis. The Task Force on Rhinosinusitis, American Academy of Otolaryngology-Head and Neck Surgery proposed major and minor factors that could be used to tentatively diagnose sinusitis. The diagnosis of sinusitis requires the presence of 1) at least two major or 2) one major and two minor factors (Table 2). Besides the clinical evaluation for sinusitis, radiological imaging has been routinely used. Four-view sinus x-rays are helpful looking for opacity, an air-fluid level, or 4 mm or more of sinus mucosal thickening. Computed tomography (CT) is noted to be more sensitive than routine radiography. In many institutions the cost of sinus x-rays and CT limited to the sinuses are comparable. Imaging studies ie. Sinus CT scans, are not recommended for the routine diagnosis of community-acquired sinusitis because of their lack of specificity. Patients with VRS have sinus CT scan abnormalities that usually can not be distinguished from those associated with acute community-acquired bacterial sinusitis (Table 1),⁷ especially early in the disease process.

The etiology of viral and bacterial causes of community-acquired sinusitis have been well established, especially for the maxillary sinuses (Table 3).⁸ The bacteriology of acute community-acquired sinusitis in adults is with three major pathogens: Streptococcus pneumoniae, Haemophilus influenzae (not type b), and Moraxella catarrhalis. In adults, gram-negative bacilli play a role (9% of cases), and anaerobes (6%) are especially important in cases associated with dental infections. In those with deficits involving humoral and cell-mediated immunity, such as in HIV, the etiologic agents are similar to those mentioned above but with an increased incidence of Pseudomonas aeruginosa and Staphlococcus spp, as determined from surgical culture. ^9,10

Treatment

Empiric therapy for acute bacterial sinusitis should be directed against the common bacterial pathogen; sinus puncture is not indicated in routine cases, and cultures of nasal drainage are not very reliable.

There are a number of antimicrobials currently available with broad activity against the usual pathogens associated with acute bacterial sinusitis. The beta-lactam antimicrobials that continue to show the best activity against penicillin sensitive and intermediately resistant strains of pneumococci, beta-lactamase-producing H. influenzae and M. catarrhalis are amoxicillin-clavulanate, cefpodoxixime, and cefuroxime. In communities where there is a high prevalence of penicillin resistant Streptococcus pneumoniae, there is also an associated resistance to many of the other commonly used antibiotics such as erythromycin, clarithomycin, and trimethoprim-sulfamethoxazole. In this situation, the oral 2^nd generation cephalosporins ie. Cefuroxime axetil may be effective. The newer quinolones ie. Levofloxacin, gatifloxacin, lomefloxacin provide excellent activity against both penicillin sensitive and resistant Streptococcus pneumoniae and other sinusitis pathogens (Table 4)¹¹, but are limited in use to adults. A 10-day course of antibiotic therapy for acute bacterial sinusitis is usually effective. With the initiation of antibiotics for bacterial sinusitis, most symptoms begin to resolve within the first 48 to 72 hours. Failure to improve should prompt consideration of bacterial resistance, noncompliance or complicated sinusitis.

REFERENCES

1. Durand M, Joseph M and Baker AN, Infections of the upper respiratory tract. In: Fauci AS, Braunwald E, Isselbacher KJ, eds. Harrison's principles of internal medicine. 14th ed., New York: McGraw Hill, 1998:179-80.
2. Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Inf Dis. 1996; 23:1209-25
3. Ahuja GS and Thompson J. What role for antibiotics in otitis media and sinusitis? Postgrad Med. 1998;104(3):93-104.
4. Runer T. Studies of mucociliary activity and blood flow in the upper airways, with special reference to endotheliins and nitric oxide. (Ph.D. thesis). Lund, Sweden: Department of Oto-Rhino-Laryngology, Head and Neck Surgery, University of Lund, 1996.
5. Gwaltney JM Jr., Phillips CD, Miller RD, Riker DK. Computed tomographic study of the common cold. N Engl J Med. 1994; 330:25-30.
6. Greve JM, Davis G, Meyer AM, et al. The major human rhinovirus receptor is ICAM-1. Cell. 1989; 56:839-47.
7. Gwaltney JM Jr., Phillips CD, Miller RD, Ricker DK. Computed tomographic study of the common cold. N Engl J Med. 1994; 330:25-30.
8. Gwaltney JM Jr. Sinusitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's principles and practice of infectious diseases. 5th ed. Vol 1, Philadephia: Churchill Livingston, 2000:676-86
9. Thompson C, Salvato P. Stroud S, et al. Etilogy of acute sinusitis in HIV infection. Int Conf AIDS. 1993:June 6-11;9(1):51 (abstract no. US-B08-6).
10. Goncalves DU, Greco DB, Toledo AC, et al. Microbiology of sinustis in AIDS. Int Conf AIDS 1994:Aug 7-12;10(2)138 (abstract no. PB0566).
11. Bartlett JG. Pocket book of infectious disease therapy. Baltimore: Williams and Wilkins, 1998.

Jacksonville Medicine / May 2000

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