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129 Branhamella–Moraxella
Moraxella catarrhalis is an important etiologic agent of otitis media in children, sinusitis in children and adults, and bronchopulmonary infection in adults with chronic obstructive pulmonary disease (COPD) or impaired host defenses.
Moraxella catarrhalis is a gram-negative unencapsulated diplococcus similar in morphology to the Neisseria. The bacterium was first described by Ghon and Pfeiffer as Micrococcus catarrhalis in 1902 and has since undergone several reclassifications. In 1970 it was placed into the genus Branhamella based on fatty acid content and DNA homology. Moraxella (Branhamella) catarrhalis is the most widely accepted nomenclature at this time.
Epidemiology
Moraxella catarrhalis is a normal inhabitant of the upper respiratory tract, but can be a pathogen in susceptible hosts. Colonization is seasonal, with an increase in prevalence during winter and spring months. Age and comorbidity are the major determinants of colonization. The mode of transmission is assumed to be direct contact with respiratory secretions or droplet spread. Approximately two-thirds of children become colonized during the first year of life. One prevalence study demonstrated that colonization with M. catarrhalis in infants occurs earlier than with Streptococcus pneumoniae or Haemophilus influenzae, and persists longer. Infants who become colonized with M. catarrhalis before 3 months of age are more likely to develop an episode of acute otitis media (AOM) or otitis media with effusion (OME) by the time they are 6 months old. Carriage rates in healthy adults are only 3% to 5%. In contrast, M. catarrhalis has been recovered in 5% to 32% of adults with COPD. Approximately half of adults with COPD who are newly colonized will develop an acute exacerbation of COPD.
The pneumococcal conjugate vaccine has altered patterns of nasopharyngeal colonization, permitting replacement with nonvaccine pneumococcal serotypes, nontypeable H. influenzae, and M. catarrhalis.
Pathogenesis
The pathogenesis of infection is complex with both host and bacterial factors determining the evolution from colonization to clinical disease. Moraxella catarrhalis expresses adhesion factors and several outer membrane proteins that facilitate preferential binding to mucosal surfaces of the upper and lower respiratory tract and to middle ear epithelial cells. Biofilm formation in sequestered sites such as the middle ear suggest its potential role in the development of AOM with effusion.
Prior colonization of the nasopharynx by M. catarrhalis appears to enhance the adherence and invasion of human epithelial cells by Streptococcus pyogenes.
Following infection, the organism has the ability to act through Toll-like receptors to induce proinflammatory cytokines in the bronchial epithelium that, in addition to causing acute exacerbations of COPD, may also be responsible for its pathogenesis. Moraxella catarrhalis also has the ability to inhibit this proinflammatory process and evade the host immune response, allowing for persistent mucosal colonization.
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