Sinusitis From Microbiology to Management - part 5 ppt

85. Brook I, Thompson D, Frazier E. Microbiology and management of chronic maxillary sinusitis. Arch Otolaryngol Head Neck Surg 1994; 120: 1317–1320. 86. Brook I. Bacteriologic features of chronic sinusitis in children. JAMA 1981; 246:967–969. 87. Finegold SM, Flynn MJ, Rose FV, Jousimies-Somer H, Jakielaszek C, McTeague M, Wexler HM, Berkowitz E, Wynne B. Bacteriologic findings associated with chronic bacterial maxillary sinusitis in adults. Clin Infect Dis 2002; 35:428–433. 88. Carenfelt C, Lundberg C. Purulent and non-purulent maxillary sinus secre- tions with respect to PO 2 , PCO 2 and pH. Acta Otolaryngol 1977; 84:138–144. 89. Brook I. Role of encapsulated anaerobic bacteria in synergistic infections. Crit Rev Microbiol 1987; 14:171–193. 90. Brook I. Bacteriology of chronic maxillary sinusitis in adults. Ann Otol Rhinol Laryngol 1989; 98:426–428. 91. Brook I. Brain abscess in children: microbiology and management. Child Neurol 1995; 10:283–288. 92. Westrin KM, Stierna P, Carlsoo B, Hellstrom S. Mucosal fine structure in experimental sinusitis. Ann Otol Rhinol Laryngol 1993; 102(8 Pt 1): 639–645. 93. Jyonouchi H, Sun S, Kennedy CA, Roche AK, Kajander KC, Miller JR, Germaine GR, Rimell FL. Localized sinus inflammation in a rabbit sinusitis model induced by Bacteroides fragilis is accompanied by rigorous immune responses. Otolaryngol Head Neck Surg 1999; 120:869–875. 94. Brook I, Yocum P. Immune response to Fusobacterium nucleatum and Prevo- tella intermedia in patients with chronic maxillary sinusitis. Ann Otol Rhinol Laryngol 1999; 108:293–295. 95. Brook I, Yocum P, Frazier EH. Bacteriology and beta-lactamase activity in acute and chronic maxillary sinusitis. Arch Otolaryngol Head Neck Surg 1996; 122:418–422. 96. Brook I, Yocum P, Shah K. Aerobic and anaerobic bacteriology of concurrent chronic otitis media with effusion and chronic sinusitis in children. Arch Oto- laryngol Head Neck Surg 2000; 126:174–176. 97. Orobello PW Jr, Park RI, Belcher L, et al. Microbiology of chronic sinusitis in children. Arch Otolaryngol Head Neck Surg 1991; 117:980–983. 98. Tinkleman DG, Silk HJ. Clinical and bacteriologic features of chronic sinusitis in children. Am J Dis Child 1989; 143:938–941. 99. Muntz HR, Lusk RP. Bacteriology of the ethmoid bullae in children with chronic sinusitis. Arch Otolaryngol Head Neck Surg 1991; 117:179–181. 100. Otten FWA, Grote JJ. Treatment of chronic maxillary sinusitis in children. Int J Pediatr Otorhinolaryngol 1988; 15:269–278. 101. Otten FWA. Conservative treatment of chronic maxillary sinusitis in children. Long term follow-up. Acta Otol Rhinol Laryngol Belg 1997; 51:173–175. 102. Don D, Yellon RF, Casselbrant M, Bluestone CD. Efficacy of stepwise proto- col that includes intravenous antibiotic treatment for the management of chronic sinusitis in children and adolescents. Otolaryngol Head Neck Surg 2001; 127:1093–1098. 174 Brook 103. Erkan M, Ozcan M, Arslan S, Soysal V, Bozdemir K, Haghighi N. Bacteriol- ogy of antrum in children with chronic maxillary sinusitis. Scand J Infect Dis 1996; 28:283–285. 104. Slack CL, Dahn KA, Abzug MJ, Chan KH. Antibiotic-resistant bacteria in pediatric chronic sinusitis. Pediatr Infect Dis J 2001; 20:247–250. 105. Goldenhersh MJ, Rachelefsky GS, Dudley J, Brill J, Katz RM, Rohr AS, Spector SL, Siegel SC, Summanen P, Baron EJ. The microbiology of chronic sinus disease in children with respiratory allergy. J Allergy Clin Immunol 1990; 85:1030–1039. 106. Wald ER, Byers C, Guerra N, et al. Subacute sinusitis in children. J Pediatr 1989; 115:28–32. 107. Brook I, Yocum P. Antimicrobial management of chronic sinusitis in children. J Laryngol Otol 1995; 109:1159–1162. 108. Finegold SM. Anaerobic bacteria in human disease. Orlando, FL: Academic Press, Inc., 1977. 109. Brook I. Pediatric Anaerobic Infections. 3rd. NY: Marcel Dekker Inc, 2002. 110. Mustafa E, Tahsin A, Mustafa O ¨ , Nedret K. Bacteriology of antrum in adults with chronic maxillary sinusitis. Laryngoscope 1994; 104:321–324. 111. Frederick J, Braude AI. Anaerobic infections of the paranasal sinuses. N Engl J Med 1974; 290:135–137. 112. Van Cauwenberge P, Verschraegen G, Van Renterghem L. Bacteriological findings in sinusitis (1963–1975). Scand J Infect Dis Suppl 1976; 9:72–77. 113. Karma P, Jokipii L, Sipila P, Luotonen J, Jokipii AM. Bacteria in chronic maxillary sinusitis. Arch Otolaryngol 1979; 105:386–390. 114. Berg O, Carenfelt C, Kronvall G. Bacteriology of maxillary sinusitis in rela- tion to character of inflammation and prior treatment. Scand J Infect Dis 1988; 20(5):511–516. 115. Fiscella RG, Chow JM. Cefixime for the treatment of maxillary sinusitis. Am J Rhinol 1991(2,5):193–197. 116. Sedallian AB, Bru JP, Gaillat J. Bacteriologic finding of chronic sinusitis. (Abstr no. P2.71). The 17th International Congress of the Management of Infection. Berlin, 1992. 117. Simoncelli C, Ricci G, Molini E, von Garrel C, Capolunghi B, Giommetti S. Bacteriology of chronic maxillary sinusitis. HNO 1992; 40:16–18. 118. Tabaqchali S. Anaerobic infections in the head and neck region. Scand J Infect Dis Suppl 1988; 57:24–34. 119. Hartog B, Degener JE, Van Benthem PP, Hordijk GJ. Microbiology of chronic maxillary sinusitis in adults: isolated aerobic and anaerobic bacteria and their susceptibility to twenty antibiotics. Acta Otolaryngol 1995; 115:672–677. 120. Ito K, Ito Y, Mizuta K, Ogawa H, Suzuki T, Miyata H, Kato N, Watanabe K, Ueno K. Bacteriology of chronic otitis media, chronic sinusitis, and paranasal mucopyocele in Japan. Clin Infect Dis 1995; 20(suppl 2):S214–S219. 121. Erkan M, Aslan T, Ozcan M, Koc N. Bacteriology of antrum in adults with chronic maxillary sinusitis. Laryngoscope 1994; 104(3 Pt 1):321–324. 122. Edelstein DR, Avner SE, Chow JM, Ouerksen RL, Johnson J, Ronis M, Rybak LP, Bierman WC, Matthews BL. Once-a-day therapy for sinusitis: Infectious Causes of Sinusitis 175 a comparison study of cefixime and amoxicillin. Laryngoscope 1993; 103:33–41. 123. Klossek JM, Dubreuil L, Richet H, Richet B, Beutter P. Bacteriology of chronic purulent secretions in chronic rhinosinusitis. J Laryngol Otol 1998; 112:1162–1166. 124. Brook I, Frazier EH. Correlation between microbiology and previous sinus surgery in patients with chronic maxillary sinusitis. Ann Otol Rhinol Laryngol 2001; 110:148–151. 125. Brook I. Bacteriology of acute and chronic frontal sinusitis. Arch Otolaryngol Head Neck Surg 2002; 128:583–585. 126. Brook I. Bacteriology of acute and chronic sphenoid sinusitis. Ann Otol Rhinol Laryngol 2002; 111:1002–1004. 127. Brook I. Bacteriology of acute and chronic ethmoid sinusitis. J Clin Microb 2005; 43:3479–3480. 128a. Bhattacharyya N, Kepnes LJ. The microbiology of recurrent rhinosinusitis after endoscopic sinus surgery. Arch Otolaryngol Head Neck Surg 1999; 125:1117–1120. 128b. Bucholtz GA, Salzman SA, Bersalona FB, Boyle TR, Ejercito VS, Penno L, Peterson DW, Stone GE, Urquhart A, Shukla SK, Burmester JK. PCR analysis of nasal polyps, chronic sinusitis, and hypertrophied turbinates for DNA encoding bacterial 16S rRNA. Am J Rhinol 2002; 16:169–173. 128c. Hamilos DL, Leung DYM, Wood R, Meyers A, Stephens JK, Barkans J, Bean DK, Kay AB, Hamid Q. Association of tissue eosinophilia and cytokine mRNA expression of granulocyte-macrophage colony-stimulating factor and interleukin-3. J Allergy Clin Immunol 1993; 91:39–48. 128d. Brook I, Frazier EH. Bacteriology of chronic maxillary sinusitis associated with nasal polyposis. J Med Microbiol 2005; 54:595–597. 129. Clement PA, Bluestone CD, Gordts F, Lusk RP, Otten FW, Goossens H, Scadding GK, Takahashi H, van Buchem FL, Van Cauwenberge P, Wald ER. Management of rhinosinusitis in children: consensus meeting, Brussels, Belgium, September 13, 1996. Arch Otolaryngol Head Neck Surg 1998; 124:31–34. 130. Brook I, Foote PA, Frazier EH. Microbiology of acute exacerbation of chronic sinusitis. Laryngoscope 2004; 114:129–131. 131. Brook I. Bacteriology of chronic sinusitis and acute exacerbation of chronic sinusitis. Annals Otolary Head Neck Surg. 132. Bach A, Boehrer H, Schmidt H, Geiss HK. Nosocomial sinusitis in ventilated patients: nasotracheal versus orotracheal intubation. Anaesthesia 1992; 47:335–339. 133. O’Reilly MJ, Reddick EJ, Black W, Carter PL, Erhardt J, Fill W, Maughn D, Sado A, Klatt GR. Sepsis from sinusitis in nasotracheally intubated patients: a diagnostic dilemma. Am J Surg 1984; 147:601–604. 134. Mevio E, Benazzo M, Quaglieri S, Mencherini S. Sinus infection in intensive care patients. Rhinology 1996; 34:232–236. 135. Caplan ES, Hoyt NJ. Nosocomial sinusitis. JAMA 1982; 247:639–641. 136. Kronberg FG, Goodwin WJ. Sinusitis in intensive care unit patients. Laryngo- scope 1985; 95:936–938. 176 Brook 137. Arens JF, LeJeune FE Jr, Webre DR. Maxillary sinusitis, a complication of nasotracheal intubation. Anesthesiology 1974; 40:415–416. 138. Brook I, Shah K. Sinusitis in neurologically impaired children. Otolaryngol Head Neck Surg 1998; 119:357–360. 139. Hahn DL, Dodge RW, Golubjatnikov R. Association of Chlamydia pneumo- niae (strain TWAR) infection with wheezing, asthmatic bronchitis, and adult- onset asthma. JAMA 1991; 266:225–230. 140. Thom DH, Grayston JT, Campbell LA, Kuo CC, Diwan VK, Wang SP. Respiratory infection with Chlamydia pneumoniae in middle-aged and older adult outpatients. Eur J Clin Microbiol Infect Dis 1994; 13:785–792. 141. Hashigucci K, Ogawa H, Suzuki T, Kazuyama Y. Isolation of Chlamydia pneumoniae from the maxillary sinus of a patient with purulent sinusitis. Clin Infect Dis 1992; 15:570–571. 142. Savolainen S, Jousimies-Somer H, Kleemola M, Ylikoski J. Serological evidence of viral or Mycoplasma pneumoniae infection in acute maxillary sinu- sitis. Eur J Clin Microbiol Infect Dis 1989; 8:131–135. 143. Gurr PA, Chakraverty A, Callanan V, Gurr SJ. The detection of M. pneumo- niae in nasal polyps. Clin Otolaryngol 1996; 21:269–273. 144. Bucholtz GA, Salzman SA, Bersalona FB, Boyle TR, Ejercito VS, Pinno L, Peterson DW, Stone GE, Urguhart A. PCR analysis of nasal polyps, chronic sinusitis, and hypertrophied turbinates for DNA encoding bacterial 16S rRNA. Am J Rhinol 2002; 16:169–173. 145. Vennewald I, Henker M, Klemm E, Seebacher C. Fungal colonization of the paranasal sinuses. Mycosis 1999; 42(suppl 2):33–36. 146. Ponikau JU, Sherris DA, Kern EB, Homburger HA, Frigas E, Gaffey TA, Roberts GD. The diagnosis and incidence of allergic fungal sinusitis. Mayo Clin Proc 1999; 74:877–884. 147. Catten MD, Murr AH, Goldstein JA, Miatre AN, Lalwani AK. Detection of fungi in the nasal mucosal using polymerase chain reaction. Laryngoscope 2001; 111:399–403. 148. Stringer SP, Ryan MW. Chronic invasive fungal rhinosinusitis. Otolaryngol Clin North Am 2000; 33:375–387. 149. Ferguson BJ. Definitions of fungal rhinosinusitis. Otolaryngol Clin North Am 2000; 33:227–235. 150. Gwaltney JM Jr. Microbiology of sinusitis. In: Druce HM, ed. Sinusitis: Pathophysiology and Treatment. New York: Marcel Dekker, 1994:41–56. 151. Morgan MA, Wilson WR, Neil HB III, Roberts GD. Fungal sinusitis in healthy and immunocompromised individuals. Am J Clin Pathol 1984; 82:597–601. 152. Jahrsdoerfer RA, Ejercito VS, Johns MME, Cantrell RW, Sydnor JE. Asper- gillosis of the nose and paranasal sinuses. Am J Otolaryngol 1979; 1:1–14. 153. Kern ME, Uecker FA. Maxillary sinus infection caused by the Homobasidiomy- cetous fungus Schizophyllum commune. J Clin Microbiol 1986; 23:1001–1005. 154. Mitchell RG, Chaplin AJ, MacKenzie DWR. Emericella nidulans in a maxil- lary sinus fungal mass. J Med Vet Mycol 1987; 25:339–341. 155. Winn RE, Ramsey PD, McDonald JC, Dunlop KJ. Maxillary sinusitis from Pseudoalles-cheria boydii. Efficacy of surgical therapy. Arch Otolaryngol 1983; 109:123–125. Infectious Causes of Sinusitis 177 156. Adam RD, Paquin ML, Petersen EA, Saubolle MA, Rinaldi MG, Corcoran JN, Solaonya RE. Phaeohyphomycosis caused by the fungal general Bipolaris and Exserohilum. Medicine 1986; 65:203–217. 157. Zieske LA, Kople RD, Hamill R. Dermataceous fungal sinusitis. Otolaryngol Head Neck Surg 1991; 105:567–577. 158. Goldstein MF, Dvorin DJ, Dunsky EH, Lesser RW, Heuman PJ, Loose JH. Allergic rhizomucor sinusitis. J Allergy Immun 1992; 90:394–404. 159. Katzenstein A, Sale SR, Greenberger PA. Pathologic findings in allergic Aspergillus sinusitis. Am J Surg Pathol 1983; 7:439–443. 160. Maran ACD, Kwong K, Mine LJR, Lamb D. Frontal sinusitis caused by Myriodontium keratinophilum. Br Med J 1985; 290:207. 161. Friedman GC, Hartwick RW, Ro JY, et al. Allergic fungal sinusitis. Report of three cases associated with dermataceous fungi. Am J Clin Pathol 1991; 96:368–372. 162. Bartynski JM, McCaffrey TV, Frigas E. Allergic fungal sinusitis secondary to dermataceous fungi—Curvularia lunata and Alternaria. Otolaryngol Head Neck Surg 1990; 103:32–39. 178 Brook 9 Antimicrobial Management of Sinusitis Itzhak Brook Departments of Pediatrics and Medicine, Georgetown University School of Medicine, Washington, D.C., U.S.A. INTRODUCTION The growing resistance to antimicrobial agents of all respiratory tract bacterial pathogens has made the m anagement of si nusitis mo re difficult. T his chapter presents the current information r egarding the antimicrobial resistance of the organisms involved in sinusitis and the approaches to antimicrobial therapy. ANTIMICROBIAL RESISTANCE To manage bacterial sinusitis is often a challenging endeavor in which selec- tion of the most appropriate antimicrobial agents remains a key decision. This has become more difficult in recent years as all the predominant bacte- rial pathogens have gradually develope d resistance to most of the commonly used antibiotics. The observed increase in bacterial resistance to antibiotics is related to their frequent use. Previous therapy can increase the prevalence of beta- lactamase-producing bacteria (BLPB). In a study of 26 children who had received seven days of therapy with penicillin, 12% harbored BLPB in their oropharyngeal flora prior to therapy (1). This increased to 46% at the conclusion of therapy, and the incidence was 27% after three months. The incidence of BLPB was high in siblings and parents of patients treated with penicillin, who pro bably acquired these organisms from the patient (2). SECTION IV. THERAPEUTIC OPTIONS 179 A greater prevalence of recovery of BLPB in the oropharynx of children occurs in the winter and a lower one in the summer (3). These changes correlated with the intake of beta-lactam antibioti cs. To monitor the local seasonal variations in the rate of recovery of BLPB in the community may help the empirical choice of antimicrobial agents, the proper and judi- cious use of which may help to control the increase of BLPB. Risk factors for the development of resistance to antimicrobial agents include prior antibiotic exposure, day care attendance, age under two years, recent hospitalization, and recurrent infection (especially in those who are very young or very old) (4,5). The variety of organisms involved in sinusitis, increasing levels of resistance to antibiotic agents, and the pheno menon of beta-lact amase ‘‘shielding’’ from antibiotic agents all contribute to the therapeutic chal- lenges associated with the management of acute and chronic sinusitis. Brook and Gober (5) identified the antimicrobial susceptibility of the pathogens isolated from patients with maxillary sinusitis who failed to respond to anti- microbial therapy and correlates it with previou s antimicrobial therapy and smoking. The data illustrated a relationship between resistance to antimicro- bials and failure of patients with sinusitis to improve. A statistically signi fi- cant higher recovery of resistant organisms was noted in those treated two to six months previously, and in those who smoked. Three major mechanisms of resistance to penicillins occur: 1. Porin channel blockage (e.g., used by Pseudomonas spp. to resist carbapenems) 2. Production of the enzyme beta-lactamase (e.g., utilized by Haemophilus influenzae and Moraxella catarrhalis). 3. Alterations in the penicillin-binding protein (e.g., used by Strepto- coccus pneumoniae). BETA-LACTAMASE PRODUCTION Bacterial resistance to the antibiotics used for the treatment of sinusitis has been increased consistently in recent years. Production of the enzyme beta- lactamase is one of the most important mechanisms of penicillin resistance. The production of the enzyme beta-lactamase is an important mechan- ism of virulence of anaerobic gram-negative bacilli as well as other aerobic and anaerobic bacteria. The production of beta-lactamase can have wider implication than just protecting the bacteria that produces the enzyme. In polymicrobial infections BLPB can ‘‘shield’’ other co-pathogens that are penicillin-susceptible (6,7) (Fig. 2 in Chap. 8). It has been hypothesized that this protection can occur when the enzyme beta-lactamase is secreted into the infected tissues or sinus fluids in sufficient quantities to break the peni- cillin’s beta-lactam ring before it can kill the susceptible bacteria, thus con- tributing to treatment failure. 180 Brook The emergence and persistence of BLPB after antibio tic therapy has implications for antimicrobial selection for in treatment of sinusitis as well as other infections of the upper respiratory tract, particularly chronic condi- tions in which patients are likely to have had recent antibiotic exposure. Clinical and laboratory studies provide supp ort for this hypothesis. Animal studies demonstrated the ability of the enzyme beta-lactamase to influence polymicrobial infections. Hackman and Wilkins (8) showed that peni- cillin-resistant strains of Bacteroides fragilis,pigmentedPrevotella and Porphyr- omonas spp., and Prevotella oralis protected a penicillin-sensitive Fusobacterium necrophorum from penicillin therapy in mice. Using a subcutaneous abscess model in mice, Brook et al. (9) demonstrated protection of group A beta-hemo- lytic streptococci (GABHS) from penicillin by B. fragilis and Prevotella melani- nogenica. C lindamycin or the combination of penicillin and clavulanic a cid (a beta-lactamase inhibitor), which are active against both GABHS and anaerobic gram-negative bacilli, were effective in eradicating the infection. Similarly, beta- lactamase–producing facultative bacteria protected a penicillin-susceptible P. melaninogenica from penicillin (10). In vitro studies have also demonstrated this phenomenon. A 200-fold increase in resistance of GABHS to penicillin was observed when it was inoculated with Staphylococcus aureus (11). An increase in resistance was also noted when GABHS was grown with Haemophilus parainfluenzae (12). When mixed with cultures of B. fragilis, the resistance of GABHS to peni- cillin increased 8500-fold (13). Several species of BLPB occur in sinusitis (Table 1). BLPB have been recovered from over one-third of patients with sinusitis (14,15). H. influenzae and M. catarrhalis are the predominant BLPB in acute sinusitis, and S. aureus, pigmented Prevotella, Porphyromonas, and Fusobacterium spp. predominate in chronic sinusitis. Table 1 Resistance to Antimicrobial Agents in Bacterial Sinusitis Bacteria Incidence (%) Resistance to penicillin (%) Acute sinusitis S. pneumoniae 30–40 20–40 H. influenzae a 25–30 30–40 M. catarrhalis a 10–15 95 Chronic sinusitis S. aureus a 10–35 95 Pigmented Prevotella a and Porphyromonas a spp. 15–30 10–60 Fusobacterium a spp. 15–40 10–60 a Resistance due to beta-lactamase production. Antimicrobial Management of Sinusitis 181 The actual activity of the enzyme beta-lactamase and the potential of the presence of the phenomenon of ‘‘shielding’’ were demonstrated in acutely and chronically inflamed sinus fluids (7). BLPB were isolated in four of 10 acute sinusitis aspirates and in 10 of 13 chronic sinusitis aspirates (Tables 2 and 3). The predominant BLPB isolated in acute sinusitis were H. influenzae and M. catarrhalis, and those found in chronic sinusitis were S. aureus, B. fragilis, and Prevotella and Fusobacterium spp. (7). ‘‘Free’’ beta- lactamase was detected in 86% of aspirates that contained these organisms, Table 2 Beta-Lactamase Detected in Four Acute Bacterial Sinusitis Aspirates Obtained from Patients Treated with Amoxicillin Patient Organism 1 a 2 a 34 S. pneumoniae þþ M. catarrhalis (beta-lactamase positive) þþ H. influenzae (beta-lactamase positive) þþ Beta-lactamase activity in pus þþ – þ a ‘‘Shielding’’ of S. pneumoniae by beta-lactamase producers is evident in patients 1 and 2. Source: Data from Ref. 7. Table 3 Beta-Lactamase Detected in Four Chronic Bacterial Sinusitis Aspirates Obtained from Patients Treated with Amoxicillin Patient Organism 1 2 3 4 S. aureus BL (þ) þþ S. pneumoniae þ Peptostreptococcus spp. þþ Propionibacterium acnes þ Fusobacterium spp. BL (þ) þþ Fusobacterium spp. BL (À) þþ Prevotella spp. BL (þ) þ Prevotella spp. BL (À) þþþ Bacteroides fragilis group BL (þ) þþ Beta-Lactamase activity in pus þþþþ a ‘‘Shielding’’ is present in all cases. Abbreviation:BL(þ), beta-lactamase–producing organism. Source: Data from Ref. 7. 182 Brook and was associated with persistence of even penicillin-susceptible pathogens despite antimicrobial therapy. Haemophilus influenzae Resistance to Antimicrobials Resistance to beta-lactams among strains of H. influenzae has increased throughout the past three decades. In the 1980s, the prevalence of beta- lactamase–produc ing H. influenzae was between 10% and 15% (16,17). Resistance among strains of H. influenzae increased steadily throughout the 1990s, and presently approximately 40% of H. influenzae strains are beta-lactamase producers. Beta-lactamase–producing strains of H. influen- zae are most prevalent in the northcentral, northeast, and southcentral regions of the United States (18). Generally, higher doses of beta-lactams are not effective in overcoming this mechanism of resistance; however, the addition of a beta-lactamase inhibi tor (e.g., clavulanic acid) shifts H. influ- enzae strains to the susceptible range [e.g., minimal inhibitory concentration (MIC) 4 mg/mL], transforming the susceptibilities to those of beta-lacta- mase–negative strains. Agents that are stable in the presence of beta-lacta- mases are another option for treating infections caused by this pathogen. Among the oral beta-lactam antibiotics, amoxicillin/clavulanate (because of the beta-lactamase inhibitor), cefixime, ceftibuten, cefdinir, and cefpodoxime are highly active against beta-lactamase–producing H. influenzae (19). Macro- lides in general have limited activity against H. influenzae;amongthethree agents (i.e., erythromycin, clarithromycin, and azithromycin), clarithromycin is least active against H. influenzae (20). Inhibition of H. influenzae by macrolides is dependent on the a bility to achieve concentrations above the MICs at the site of in fection. Based on pharmacokinetic/pharmacodynamic (PK/PD) breakpoints, the MICs of v irtually all H. influenzae strains in the 1998 surveil- lance study were below PK/PD breakpoints (i.e., res istant) for erythromycin, clarithromycin, and azithromycin. Furthermore, azithromycin f ailed t o e radi- cate 61% of H. influenzae from the middle ear of children with otitis media (21). Resistance to trimethoprim-sulfamethoxazole (TMP/SMX) was exhibited among 24% of isolates. Fluoroquinolones, particularly the newer agents, ar e very active against H. influenzae, with relatively no resistance according to the recent surveillance data (20). Moraxella catarrhalis Resistance to Antimicrobials Virtually all strains of M. catarrhalis produce beta-lactamase. The 1998 pre- valence among outpatient isolates for beta-lactamase–producing M. catarrhalis was 98% (19 ). At PK/PD breakpoints, 100 % of strai ns were s usceptible to amoxicillin/clavulanate, fluoroquinolones, macrolides, doxycycline, and cefix- ime. High levels of resistance were exhibited toward TMP/SMX, cefaclor, loracarbef, cefprozil, and amoxicillin. Antimicrobial Management of Sinusitis 183 [...]... TMP-SMX (Bactrim, Septra) Adult dosage 250 50 0 mg bid 250 50 0 mg bid 200–400 mg bid 300 mg bid 50 0 mg tid or 8 75 mg bid 50 0 mg tida or 8 75 mg or 2000 mg (XR) bida Duration of therapy for acute sinusitis Pediatric (days) dosage (mg/kg) 7 .5 15 bid 10– 15 bid 5 bid 7 bid/14 qd 20– 45 bid 10 10 10 10 14 22 .5 or 45 (ES600) bid 10 800 mg qd NA 5 250 mg qd 50 0 mg bid 10 day 1, then 5 qd 7 .5 bid 50 0 mg qd 50 0... Frazier EH Microbiology and management of chronic maxillary sinusitis Arch Otolaryngol Head Neck Surg 1994; 120:1317–1320 55 Brook I, Yocum P Management of chronic sinusitis in children J Laryngol Otol 19 95; 109:1 159 –1162 56 Decker CF Sinusitis in the immunocompromised host Curr Infect Dis Rep 1999; 1:27–32 10 Medical Management of Acute Sinusitis Dennis A Conrad Division of Infectious Diseases, Department... Infect Dis J 1996; 15: 255 – 259 43 Schentag JJ, Gilliland KK, Paladino JA What have we learned from pharmacokinetic and pharmacodynamic theories? Clin Infect Dis 2001; 32(suppl 1): S39–S46 44 Brook I, Frazier EH, Foote PA Microbiology of the transition from acute to chronic maxillary sinusitis J Med Microbiol 1996; 45: 372–3 75 45 Brook I, Frazier EH, Foote PA Microbiology of chronic maxillary sinusitis: comparison... will help to Amoxicillin Amoxicillin-clavulanate Cephalexin (first-generation) Cefactor (second-generation) Cefprozil (second-generation) Cefuroxime axetil (second-generation) Cefpodoxime (second-generation) Cefdinir (second-generation) Cefixime (third-generation) Ceftibuten (third-generation) Loracarbef Ceftriaxoneb Erythromycin-sulfisoxazole Trimethoprim-sulfamethoxazole Antimicrobial agent Pen-IR þ þ... stronger affinity to these enzyme-binding sites First- and second-generation fluoroquinolones bind primarily to DNA gyrase or DNA topoisomerase IV, whereas the third-generation fluoroquinolones generally bind strongly to both DNA gyrase and DNA topoisomerase IV Thus, a single point mutation in DNA gyrase or DNA topoisomerase IV generally affects first- and second-generation fluoroquinolones to a greater extent... approved for clinical use It is structurally related to the macrolides, but has a low propensity to select for or induce resistance to macrolide-lincosamide-streptogramin antibacterials (38) In vitro, telithromycin is effective against multi-drug-resistant S pneumoniae (regardless of the presence of macrolide-resistant determinants Antimicrobial Management of Sinusitis 191 [erm(B), mef(A)]), GABHS, M catarrhalis,... of maxillary sinusitis Scand J Infect Dis 19 75; 7: 259 –264 47 Gwaltney JM Jr Acute community-acquired sinusitis Clin Infect Dis 1996; 23:209–2 25 48 Wald ER, Chiponis D, Leclesma-Medina J Comparative effectiveness of amoxicillin and amoxicillin–clavulanate potassium in acute paranasal sinus infection in children: a double-blind, placebo-controlled trial Pediatrics 1998; 77:7 95 800 49 Spector SL, Bernstein... penicillinresistant organisms from children Pediatr Infect Dis J 1997; 16: 255 – 256 4 McCracken GH Jr Considerations in selecting an antibiotic for treatment of acute otitis media Pediatr Infect Dis J 1994; 13:1 054 –1 057 5 Brook I, Gober AE Resistance to antimicrobials used for therapy of otitis media and sinusitis: effect of previous antimicrobial therapy and smoking Ann Otol Rhinol Laryngol 1999; 108:6 45 647 6 Brook... the management of rhinosinusitis in children is noteworthy for providing recommendations concerning the place for surgery in the management of sinusitis (7) Medical Management of Acute Sinusitis 207 Table 3 Management of Acute Sinusitis in Children The diagnosis of acute bacterial sinusitis in children is clinical, and is based on either persistence or severity of upper respiratory tract symptoms... commonly used to treat sinusitis (Table 4) The term drug-resistant S pneumoniae refers to strains with penicillin MICs ! 0.12 mg/mL that also exhibit resistance to at least two other antimicrobial classes The susceptibility of S pneumoniae isolates to other antimicrobials is closely correlated to its susceptibility to penicillin However, these strains are susceptible to parenteral third-generation cephalosporins . Wymox) 50 0 mg tid or 8 75 mg bid 20– 45 bid 14 Amoxicillin-clavulanate (Augmentin) 50 0 mg tid a or 8 75 mg or 2000 mg (XR) bid a 22 .5 or 45 (ES600) bid 10 Ketolides Telithromycin (Ketek) 800 mg qd NA 5 Macrolides Azithromycin. of GABHS to peni- cillin increased 850 0-fold (13). Several species of BLPB occur in sinusitis (Table 1). BLPB have been recovered from over one-third of patients with sinusitis (14, 15) . H. influenzae and. aureus Antimicrobial agent Pen-S Pen-IR BLÀ BLþ BLþ Pen-S Pen-R Pen-R a Amoxicillin þþþÀ À þÀÀ Amoxicillin-clavulanate þþþþ þ þþþ Cephalexin (first-generation) þÀÆÀ À þÀþ Cefactor (second-generation) ÆÀþÆ