Report of the UK Cystic Fibrosis Trust Antibiotic Working Group

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• It is important to assess the clinical response after itraconazole withdrawal to assess whether it isstill beneficial (e.g., prevents relapse and is corticosteroid-sparing) [C].• For patients receiving itraconazole, liver function tests should be obtained before therapy andshould be repeated whenever there is any suspicion of liver dysfunction. Routine liver functiontesting after 1 month and then every 3–6 months if therapy continues should be considered [C].• Concomitant medications should be meticulously reviewed to avoid a drug-drug interaction anddoses of concomitant medications and itraconazole should be adjusted accordingly. This mayrequire determination of serum concentrations of concomitant drugs and/or itraconazole [C].• Determination of itraconazole concentrations should also be considered when there is a lack ofclinical response or if there is concern about adequate drug absorption or patient compliance.Blood should be drawn 4 hours after a dose; at steady state, achieved during the second week oftherapy, random samples may be useful [C].• For those whom antifungal therapy is indicated and there is evidence of poor absorption ofitraconazole, oral voriconazole could be considered as an alternative. The oral dosage schedule isas follows:• Children
7.9.6 Recommendations for invasive pulmonary aspergillosis, aspergillomas, andaspergillus bronchitis.• The optimum therapy for non-ABPA presentations of Aspergillus sp. in persons with CF remainsuncertain. The options for systemic antifungal therapy include amphotericin B (non-lipid orlipid preparations), voriconazole or caspofungin. In some presentations e.g., TBA, surgicaldebidement may also be of benefit [C].7.9.7 Other fungiOther fungi are an increasingly recognised complication of CF. Scedosporium apiospermum isfrequently isolated from persons with CF and has been associated with a symptom complex similar toABPA. 174 Unlike Aspergillus sp. it has been difficult to isolate from the environment. Patients canbecome chronically colonised with the same strain 175 [3] which can persist in spite of antifungaltherapy. It is also capable of causing invasive disease with high mortality post lung-transplant. 176 [3]Therapy is compromised by its resistance to many antifungal agents, including itraconazole andamphotericin B. 177 [3] Many isolates appear susceptible in vitro to voriconazole 178;179 [3] but this hasbeen associated with clinical failure in patients 180 and in animal models. 181 [3] In vitro data suggeststhat posaconazole may also be a possible treatment. 182 [3] Another fungus increasingly observed isExophiala dermatitidis. However, its significance in CF remains uncertain. 1837.9.8 Recommendations for unusual fungal infection• If considered clinically significant, Scedosporium apiospermum should be treated withvoriconazole or posaconazole [C].7.10 References1. Govan JR, Hughes JE, Vandamme P. Burkholderia cepacia: medical, taxonomic and ecological issues. J Med Micro1996;45:395–407.2. LiPuma JJ. Burkholderia cepacia. Management issues and new insights. Clin Chest Med 1998;19:473–86.3. Jones AM, Dodd ME, Webb AK. Burkholderia cepacia: current clinical issues, environmental controversies andethical dilemmas. Eur Respir J 2001;17:295–301.4. Coenye T, Vandamme P, Govan JR, LiPuma JJ. Taxonomy and identification of the Burkholderia cepacia complex.J Clin Microbiol 2001;39:3427–36.5. Whiteford ML, Wilkinson JD, McColl JH, Conlon FM, Michie JR, Evans TJ et al. Outcome of Burkholderia(Pseudomonas) cepacia colonisation in children with cystic fibrosis following a hospital outbreak. Thorax1995;50:1194–8.6. Muhdi K, Edenborough FP, Gumery L, O’Hickey S, Smith EG, Smith DL et al. Outcome for patients colonisedwith Burkholderia cepacia in a Birmingham adult cystic fibrosis clinic and the end of an epidemic. Thorax1996;51:374–7.7. Hutchison ML,.Govan JR. Pathogenicity of microbes associated with cystic fibrosis. Microbes & Infection1999;1:1005–14.8. McCloskey M, McCaughan J, Redmond AO, Elborn JS. Clinical outcome after acquisition of Burkholderia cepaciain patients with cystic fibrosis. Ir J Med Sci 2001;170:28–31.9. Mahenthiralingam E, Vandamme P, Campbell ME, Henry DA, Gravelle AM, Wong LT et al. Infection withBurkholderia cepacia complex genomovars in patients with cystic fibrosis: virulent transmissible strains ofgenomovar III can replace Burkholderia multivorans. Clin Infect Dis 2001;33:1469–75.10. Jones AM, Dodd ME, Govan JR, Barcus V, Doherty CJ, Morris J et al. Burkholderia cenocepacia and Burkholderiamultivorans: influence on survival in cystic fibrosis. Thorax 2004;59:948–51.11. Manno G, Dalmastri C, Tabacchioni S, Vandamme P, Lorini R, Minicucci L et al. Epidemiology and clinicalcourse of Burkholderia cepacia complex infections, particularly those caused by different Burkholderia cenocepaciastrains, among patients attending an Italian Cystic Fibrosis Center. J Clin Microbiol 2004;42:1491–7.Cystic Fibrosis Trust 7.9.6March 2009
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4. ORAL ANTIBIOTICS IN CYSTIC FIBRO
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7. OTHER INFECTIONS7.1 Management o
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GRADING SCHEME FOR LEVELS OF EVIDEN
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SUMMARY•All young children with c
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In 1989 the Copenhagen centre recom
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These bacteria can be harmless comm
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2.7 Clinical relevance of in vitro
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Page 21 and 22: 3.1 Introduction3. IDENTIFICATION O
Page 23 and 24: Table 2: Laboratory techniques and
Page 25 and 26: 20. Hoppe JE, Theurer MU, Stern M.
Page 27 and 28: 4.2.4 Recommendations for treatment
Page 29 and 30: 4.5 Use of oral antibiotics at time
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Page 33 and 34: 5.1 Introduction5. NEBULISED ANTIBI
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Page 42 and 43: 5.16 Nebuliser/compressor systems f
Page 44 and 45: 19. Ratjen F, Walter H, Haug M, Mei
Page 46 and 47: 69. Pitchford KC, Corey M, Highsmit
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Page 50 and 51: Drug Route Age/weight DoseFrequency
Page 52 and 53: much sooner. A minimum of 10-14 day
Page 54 and 55: 6.8 References1. Armstrong DS, Grim
Page 56 and 57: 7. OTHER INFECTIONS7.1 Management o
Page 58 and 59: 7.2 Respiratory infection with meti
Page 60 and 61: Table 7.2 Published data on eradica
Page 62 and 63: 7.4.2 Recommendations• Given the
Page 64 and 65: although not all authors have found
Page 66 and 67: Table 7.3 Drugs for treatment of My
Page 68 and 69: 7.9.2 Diagnosis of ABPAThe Cystic F
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Page 74 and 75: 57. Ballestero S, Virseda I, Escoba
Page 76 and 77: 107. Deerojanawong J, Sawyer SM, Fi
Page 78 and 79: 155. Stevens DA, Moss RB, Kurup VP,
Page 80 and 81: 8. PHARMACOPOEIAOriginally based on
Page 82 and 83: 8.3 Treatment of more severe exacer
Page 84 and 85: Co-amoxiclav orallyAge Dose Frequen
Page 86 and 87: Cefotaxime intravenouslyAge Dose Fr
Page 88 and 89: 8.7 Treatment of Pseudomonas aerugi
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Page 92 and 93: Amikacin intravenouslyAge Dose Freq
Page 94 and 95: 8.10 Chronic oral anti-pseudomonal
Page 96 and 97: TemocillinAge Dose Frequency>12year
Page 98 and 99: Liposomal Amphotericin (“Ambisome
Page 100 and 101: 9. ANTIBIOTIC-RELATED ALLERGIES AND
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Report of the UK Cystic Fibrosis Trust Antibiotic Working Group

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