Biofilm and Planktonic Antibiotic Resistance in Patients With Acute Exacerbation of Chronic Rhinosinusitis.

INTRODUCTION: The recalcitrant nature of patients with acute exacerbation of chronic rhinosinusitis (AECRS) potentially involves persisting colonization of the sinonasal mucosa by bacterial biofilms. Biofilms are known to be highly resistant to antibiotics, which may trigger or maintain chronic inflammation in the sinonasal mucosa. However, little is known about the relationship between the minimum inhibitory concentration (MIC) and antibiofilm concentrations of bacteria obtained from AECRS patients. MATERIAL AND METHODS: Thirty bacterial strains from 25 patients with AECRS were identified and underwent MIC determination (VITEK® 2). The planktonic isolates were submitted to an in vitro formation of biofilms (Modified Calgary Biofilm Device) and determination of minimum biofilm inhibitory concentration (MBIC) and minimum biofilm eradication concentration (MBEC) for amoxicillin, amoxicillin/clavulanic acid, clarithromycin, and levofloxacin. MIC of the planktonic forms was compared with MBIC and MBEC levels, according to the breakpoints established by the Clinical Laboratory Standards Institute guidelines. RESULTS: The main bacteria retrieved was S. aureus (60%), followed by other Gram-positive and Gram-negative bacteria in lower frequencies. 76.7% of strains formed biofilm in vitro (n=23/30). The planktonic isolates presented high rates of resistance for amoxicillin (82.6%) and clarithromycin (39.1%), and lower rates for amoxicillin/clavulanic acid (17.4%). The biofilm-forming bacteria counterparts presented higher levels of MBIC and MBEC compared to the MIC levels for amoxicillin, amoxicillin/clavulanic acid, and clarithromycin. Levofloxacin was highly effective against both planktonic and biofilm forms. Planktonic resistant forms were associated with levels of antibiofilm concentrations (MBIC and MBEC). CONCLUSIONS: Biofilm-forming bacteria from AECRS patients are prevalent, and biofilm forms are highly resistant to antibiotics compared to their planktonic counterparts. Antibiotic resistance observed in planktonic forms is a good indicator of biofilm resistance, although near 20% of susceptible planktonic bacteria can produce antibiotic tolerant biofilms.

Amoxicillin-clavulanate for patients with acute exacerbation of chronic rhinosinusitis: a prospective, double-blinded, placebo-controlled trial.

BACKGROUND: The management of acute exacerbation of chronic rhinosinusitis (AECRS) is still under debate, especially because there are no adequate studies to support a best-evidence treatment for this condition. Antibiotic use for AECRS has been recommended based on extrapolation of data from acute rhinosinusitis (ARS) or non-placebo-controlled studies. This study aimed to evaluate whether antibiotic therapy modifies the course of AECRS in a randomized, placebo-controlled study. METHODS: Patients with AECRS were randomized in a double-blinded manner (2:1 ratio) to receive either amoxicillin-clavulanate 875 mg/125 mg twice daily (BID) (AMX-CLAV, n = 21) or placebo capsules (n = 11) during 14 days. All patients were also treated with mometasone furoate and nasal washes with saline. Global sinonasal symptoms (Severity Symptom Assessment [SSA]), quality of life (22-item Sino-Nasal Outcome Test [SNOT-22]), nasal endoscopic score (Lund-Kennedy), and microbiological evaluation were compared to evaluate the efficacy of antibiotic therapy in AECRS. RESULTS: Despite the majority of bacteria cultured from the middle meatus swab were sensitive for AMX-CLAV (84%), both AMX-CLAV and placebo-treated groups presented the same clinical course, with no difference between groups. Both groups exhibited overall improvement of symptoms on day 14 compared to day 0 (p < 0.01), especially the items "nasal secretion" and "nasal obstruction" (p < 0.05). We also observed the same evolution of nasal endoscopic and quality of life scores between placebo and AMX-CLAV. CONCLUSION: We concluded that AMX-CLAV for 14 days did not change the clinical course of AECRS compared with placebo. The addition of an oral antibiotic to ongoing topical intranasal steroid spray may not provide additional benefit during management of AECRS.

Atopia e hipertrofia adenoamigdaliana em pacientes respiradores bucais em um centro de referencia / Atopy and adenotonsillar hypertrophy in mouth breathers from a reference center

O respirador bucal utiliza a cavidade oral como principal via durante a respiração. Dentre as principais causas, destacam-se: as hipertrofias adenoamigdalianas e as doenças inflamatórias como a rinite alérgica. OBJETIVO: Verificar a presença de atopia, os principais alérgenos envolvidos e verificar a coexistência de atopia com o grau de hipertrofia das tonsilas faríngeas e palatinas, em pacientes respiradores bucais. MÉTODO: Estudo de coorte histórico com corte transversal com revisão de 308 prontuários de pacientes acompanhados em um centro do respirador bucal de um hospital terciário, no período de 2008 a 2010. Foram coletados dados sobre a história clínica de respirador bucal e realizados exames clínico otorrinolaringológico, nasofibroscópico e teste cutâneo de leitura imediata aos aeroalérgenos. RESULTADOS: Dos 308 pacientes, 36% apresentaram positividade no teste alérgico, sendo que dos atópicos 95% foram positivos para ácaros. Do total de pacientes, 46% apresentaram hipertrofia adenoideana. Destes, 37% são atópicos e 47% apresentaram hipertrofia amigdaliana e, destes, 33% são atópicos. CONCLUSÃO: Nenhuma correlação direta entre atopia e o grau de aumento das tonsilas palatinas e faríngeas foi observada nos pacientes respiradores bucais avaliados. .

Mouth breathers use the oral cavity as their principal breathing route. The main causes include: adenotonsillar hypertrophy and inflammatory diseases such as allergic rhinitis. OBJECTIVE: To look for atopy, the main allergens involved and to check for atopy as a comorbidity with the degree of hypertrophy of the tonsils and adenoids in mouth breathers. METHOD: A historical cohort study with cross-sectional review of 308 medical charts of patients treated at a mouth breather care center of a tertiary hospital in the period of 2008-2010. We collected data on the mouth breather's clinical history and we ran otolaryngological exams, flexible nasal endoscopy and skin prick test to aeroallergens. RESULTS: Of 308 patients, 36% were positive on allergy testing, with 95 % of atopic patients being positive for mites. Among all patients, 46% had adenoid hypertrophy; of these, 37% were atopic and 47% had tonsillar hypertrophy, and among these, 33% were atopic. CONCLUSION: We found no direct correlation between atopy and the degree of tonsils and adenoid hypertrophy observed among the mouth-breathing patients assessed. si. .

Atopy and adenotonsillar hypertrophy in mouth breathers from a reference center.

UNLABELLED: Mouth breathers use the oral cavity as their principal breathing route. The main causes include: adenotonsillar hypertrophy and inflammatory diseases such as allergic rhinitis. OBJECTIVE: To look for atopy, the main allergens involved and to check for atopy as a comorbidity with the degree of hypertrophy of the tonsils and adenoids in mouth breathers. METHOD: A historical cohort study with cross-sectional review of 308 medical charts of patients treated at a mouth breather care center of a tertiary hospital in the period of 2008-2010. We collected data on the mouth breather's clinical history and we ran otolaryngological exams, flexible nasal endoscopy and skin prick test to aeroallergens. RESULTS: Of 308 patients, 36% were positive on allergy testing, with 95 % of atopic patients being positive for mites. Among all patients, 46% had adenoid hypertrophy; of these, 37% were atopic and 47% had tonsillar hypertrophy, and among these, 33% were atopic. CONCLUSION: We found no direct correlation between atopy and the degree of tonsils and adenoid hypertrophy observed among the mouth-breathing patients assessed. si.