The Anthonisen classification system helps to establish a diagnosis of ABECB
. It uses 3 types of exacerbations to identify patients likely infected with bacterial pathogens, based on the presence of the clinical symptoms of increased dyspnea, sputum volume, and sputum purulence (TABLE 2).
The authors concluded that "the safety of new agents cannot be known with certainty until a drug has been on the market for many years." With unproven safety profiles, are new agents the best choice for ABECB therapy?
For optimal therapy of ABECB, macrolides, amoxicillin/ clavulanate, or new agents may not be the best choice.
Criteria for Optimized Therapy of ABECB (6) Evidence based Therapeutic Safe Cost effective Optimal dosage and duration REFERENCES: (1.) Grossman RF.
Similar to ABS, variables associated with treatment failure in ABECB include recent antibiotic use and significant comorbidities, such as cardiac disease, which can increase the risk of treatment failure more than 2-fold.
Treatment failure in ABECB has been shown to result in increased use of health care resources caused by additional physician visits, further diagnostic tests, and repeated antibiotic treatments, (5,6) Significant comorbidity, such as cardiac disease, chronic corticosteroid administration, severely impaired underlying lung function, use of supplemental oxygen, frequent purulent exacerbations of COPD, malnutrition, advanced age, generalized debility, and chronic mucous hypersecretion (TABLE 2) all increase the costs associated with treatment failure and hospitalization.
As seen in ABS and ABECB, one of the most important risk factors for infection with a resistant organism is recent antibiotic therapy, including [beta]-lactam therapy within the past 3 months.
(4) Treatment with appropriate antibiotics significantly decreases bacterial airway burden, suggesting that appropriate antibiotic use can reduce the symptoms of ABECB and decrease the risk of progression to a more severe infection.
(10,12) High-risk ABECB patients commonly present with additional risk factors, such as poor underlying lung function ([FEV.sub.1] <50% predicted) or cardiac disease, experience 4 or more exacerbations per year, use home oxygen, take oral steroids chronically, or have taken an antibiotic in the past 3 months.
TABLE 1 Bacterial distribution associated with RTIs Prevalence (%) Pathogen ABS ABECB CAP Streptococcus pneumoniae 20-43 3-25 20-60 Haemophilus influenzae 22-35 14-36 3-10 Moraxella catarrhalis 2-10 7-21 -- Staphylococcus aureus 0-8 3-20 3-5 Streptococcus spp 3-9 -- -- Anaerobes 0-9 -- -- Pseudomonas spp -- 1-15 -- Haemophilus parainfluenzae -- 2-28 -- Enterobacteriaceae spp -- 5-33 -- Mycoplasma pneumoniae -- -- 1-6 Chlamydia pneumoniae -- -- 4-6 Legionella spp -- -- 2-8 Gram-negative bacteria -- -- 3-10 ABECB, acute bacterial exacerbation of chronic bronchitis; ABS, acute bacterial rhinosinusitis; CAP, community-acquired pneumonia.
Antibiotic therapy for ABS, ABECB, and CAP is simplified somewhat because the distributions of bacterial pathogens associated with each infection overlap substantially.
Atypical respiratory pathogens, most notably Chlamydophila (previously Chlamydia) pneumoniae, account for about 5% to 10% of organisms isolated from patients with ABECB. (17) Patients with CAP also tend to be infected with the above-listed typical pathogens as well as the atypical Mycoplasma pneumoniae, C pneumoniae, and Legionella pneumophila.