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Moraxella catarrhalis infections

Timothy F Murphy, MD
Section Editor
John G Bartlett, MD
Deputy Editor
Sheila Bond, MD


Moraxella catarrhalis is a gram-negative diplococcus that commonly colonizes the upper respiratory tract, particularly in children. For much of the last century, the bacterium was regarded as a commensal. However, research has established that M. catarrhalis is an important and common human respiratory tract pathogen, in particular as a cause of acute otitis media in children and of exacerbations in adults with chronic obstructive pulmonary disease (COPD).

The epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, and prevention of infections caused by M. catarrhalis will be reviewed here. Acute otitis media, COPD, and rhinosinusitis are discussed in detail separately. (See "Acute otitis media in children: Epidemiology, microbiology, clinical manifestations, and complications" and "Acute otitis media in children: Diagnosis" and "Acute otitis media in children: Treatment" and "Acute otitis media in adults" and "Management of infection in exacerbations of chronic obstructive pulmonary disease" and "Acute bacterial rhinosinusitis in children: Clinical features and diagnosis" and "Acute bacterial rhinosinusitis in children: Microbiology and treatment" and "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis" and "Uncomplicated acute sinusitis and rhinosinusitis in adults: Treatment".)


M. catarrhalis is an exclusively human pathogen with an ecologic niche in the human upper respiratory tract.


Prevalence of colonization — The prevalence of M. catarrhalis colonization is highly dependent on age. Whereas healthy adults are rarely colonized with this organism, most infants have upper respiratory tract colonization at some time in the first several years of life [1,2]. Substantial geographic variation in the rate of colonization has been observed. As an example, a study in Buffalo, New York, showed that 66 percent of infants were colonized at least once in the first year of life, whereas a study in Göteborg, Sweden, showed colonization of approximately one-half that rate [3,4]. Active turnover of colonizing strains occurs. Differences in colonization rates are affected by multiple factors, including living conditions, hygiene, household smoking, and genetics of the population, among others.

Impact of pneumococcal vaccination on colonization — Because the pathogenesis of bacterial otitis media involves the migration of bacteria from the nasopharynx to the middle ear via the eustachian tube, patterns of nasopharyngeal colonization directly affect the distribution of pathogens that cause otitis media. The widespread administration of pneumococcal conjugate vaccines is resulting in changing patterns of nasopharyngeal colonization in populations with vaccination programs. Since the introduction of the 7-valent pneumococcal conjugate vaccine as part of routine childhood immunizations in the United States in 2000, colonization by vaccine serotypes of Streptococcus pneumoniae has decreased, and colonization by nonvaccine serotypes of S. pneumoniae, nontypeable Haemophilus influenzae, and M. catarrhalis has increased, resulting in a shift of pathogens that cause otitis media [5,6]. Similar changes in the rates of colonization with these organisms have been observed in other regions [7], and changes in the profile of microorganisms colonizing the nasopharynx have also been observed following the introduction of the 13-valent pneumococcal vaccine in the United States in 2010 and the 10-valent vaccine in Europe in 2009 [8-10]. One study demonstrated an increased prevalence of nasopharyngeal colonization by M. catarrhalis during episodes of otitis media in children who received the 7-valent pneumococcal conjugate vaccine, compared with the prevalence in children with otitis media before introduction of the vaccine [11]. Similar shifts have been observed in children and adults with sinusitis [12,13].

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Literature review current through: Sep 2017. | This topic last updated: Aug 15, 2017.
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