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The Burden and Outcome of Respiratory Tract Infection in Australian and Aboriginal Children

Leach, Amanda J. PhD*; Morris, Peter S. PhD*†

The Pediatric Infectious Disease Journal: October 2007 - Volume 26 - Issue 10 - p S4-S7
doi: 10.1097/INF.0b013e318154b238

Abstract: The burden of otitis media in developing and disadvantaged populations is substantial. This article looks at that burden in developed affluent and indigenous populations (in Australia). A model is presented to explain the high prevalence of chronic suppurative otitis media in indigenous populations, and an assessment of efforts to improve these outcomes if not prevent these infections is provided. Lastly, various international guidelines for managing acute otitis media are compared.

From the *Ear and Respiratory Unit, Child Health Division, Menzies School of Health Research, and Charles Darwin University, Darwin, Northern Territory, Australia; and †Flinders University, Adelaide, South Australia, Australia.

Accepted for publication July 17, 2007.

Amanda J. Leach, PhD has nothing to disclose with regards to commercial support. Dr. Leach is planning to discuss unlabeled/investigational uses of commercial products.

Peter Morris, MBBS, FRACP, PhD has nothing to disclose with regards to commercial support.

Address for correspondence: Amanda J. Leach, PhD, Menzies School of Health Research, John Matthews Building, Royal Darwin Hospital, P.O. Box 41096, Casuarina, Northern Territory, Australia. E-mail:

CME Overview

Accreditation and Certification

This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of Boston University School of Medicine and The Physicians Academy for Clinical and Management Excellence. Boston University School of Medicine is accredited by the ACCME to provide continuing medical education for physicians.

Boston University School of Medicine designates this educational activity for a maximum of 1.25 AMA PRA Category 1 Credits TM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Statements of credit will be provided by mail within six weeks following activity participation and upon completion and return of evaluation form to Boston University School of Medicine at BUSM CME, E.PCV11PA07, 715 Albany St., A-305, Boston, MA 02118, Fax: 617-638-4905. For CME questions, please call BUSM CME at 617-638-4605.

Intended Audience

This activity has been designed for adult and pediatric clinical infectious disease specialists, microbiologists, and vaccinologists. It will provide material that is relevant to the concerns of clinicians and researchers who are interested in the treatment and management of infectious disease and how these strategies impact on patient outcomes.

Educational Needs Addressed

Acute otitis media (AOM) is one of the most common afflictions affecting children under the age of 5 years of age. In developed countries, nearly every child becomes a nasopharyngeal carrier of S. pneumoniae (SP) during the first year of life and the pathogen persists in the nasopharynx, which is significant as most cases of AOM result from a middle ear reflux from the nasopharynx. In developing countries, SP is one of the most notable bacterial pathogens for children under 6 months of age. Based upon available data, SP is estimated to kill one million children under five years of age worldwide. New vaccines are needed to provide the protective immunity necessary against the large number of SP serotypes that exist globally. The changing microbiology of SP disease, with a shift from SP to non-typeable H. influenzae (NTHi), likely based on the impact of currently available vaccine, demonstrates the even greater need for education on the use of existing and emergent conjugate vaccines in treating AOM. Success will also require expanded coverage against additional otopathogens, especially NTHi. A meaningful educational and action-oriented approach will enhance the global ability to prevent and treat AOM and its sequelae.

Educational Objectives

Upon completion of this educational activity participant should be better able to:

Release date   October 1, 2007   Expiration date   September 30, 2008

Estimated Time to Complete This Activity

1 hour and 15 minutes

Method of Participation

In order to successfully complete this activity, participants are required to read the entire supplement and complete and submit the test answer sheet by September 30, 2008. CME credit will be awarded provided a score of 70% or better is achieved. Statements of credit will be provided by mail within six weeks of receipt of the test answers to those who successfully complete the examination.

Course Director

Stephen I. Pelton, MD

Chief, Pediatric Infectious Disease

Boston Medical School

Professor of Pediatrics and Epidemiology

Boston University School of Medicine


Lauren O. Bakaletz, PhD

Professor of Pediatrics

The Ohio State University, College of Medicine

Director, Center for Microbial Pathogenesis

Columbus Children's Research Institute

Janet R. Casey, MD

Legacy Pediatrics, PLLC

University of Rochester, School of Medicine and Dentistry

Amanda J. Leach, PhD

Ear and Respiratory Health Unit

Tropical and Infectious Diseases Division

Menzies School of Health Research

Charles Darwin University

Eugene Leibovitz, MD

Pediatric Infectious Disease Unit

Soroka Medical Center and The Faculty of Health Sciences

Ben-Gurion University of the Negev

Peter S. Morris, MBBS, FRACP, PhD

Deputy Leader of Child Health Division

Menzies School of Health Research

Charles Darwin University

Associate Professor of Pediatrics

Flinders University

Michael E. Pichichero, MD

Professor of Microbiology and Immunology

Professor of Pediatrics and Professor of Medicine

University of Rochester, School of Medicine and Dentistry

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Boston University School of Medicine asks all individuals involved in the development and presentation of Continuing Medical Education (CME) activities to disclose all relationships with commercial interests. This information is disclosed to CME activity participants. Boston University School of Medicine has procedures to resolve apparent conflicts of interest. In addition, faculty members are asked to disclose when any discussion of unapproved use of pharmaceuticals and devices is being discussed.


Stephen I. Pelton, MD has indicated that he has received grant/research support from Sanofi-Aventis; serves as a consultant for GlaxoSmithKline and Wyeth; and has been on the Speakers Bureau for Sanofi-Aventis. Dr. Pelton does not plan to discuss off-label/investigational uses of commercial products.

Amanda J. Leach, PhD has no relevant financial relationships to disclose. Dr. Leach does not plan to discuss off-labeled/investigational uses of commercial products.

Peter S. Morris, PhD has no relevant financial relationships to disclose. Dr. Morris does not plan to discuss off-label/investigational uses of commercial products.

Eugene Leibovitz, MD has no relevant financial relationships to disclose. Dr. Leibovitz does not plan to discuss off-label/investigational uses of commercial products.

Michael E. Pichichero, MD has indicated that he has received grant/research support from Abbott, GlaxoSmithKline, MedImmune, Sanofi-Aventis, and Sanofi-Pasteur; Honoraria from Abbott, GlaxoSmithKline, Sanofi-Aventis, and Sanofi-Pastuer. Dr. Pichichero does not plan to discuss off-label/investigational uses of commercial products.

Janet R. Casey, MD has indicated that she has been a single-day consultant for Abbott, GlaxoSmithKline, Sanofi-Aventis, and Sanofi-Pasteur. Dr. Casey does not plan to discuss off-label/investigational uses of commercial products.

Lauren Bakaletz, PhD has indicated that she has received grant/research support from GlaxoSmithKline Biologicals. Dr. Bakaletz does not plan to discuss off-label/investigational uses of commercial products.

Planning Committee: Mary Deering, Barry A. Fiedel, PhD, Heidi J. Katz, RPh, Amy Klopfenstien, MS and Kelly McPherson of Physicians Academy, along with Julie White, MS, Elizabeth Gifford and Elizabeth D. Barnett, MD of Boston University School of Medicine have no relevant financial relationships to disclose.

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Otitis media (OM) is a common but complex disease affecting many children and families across the globe. The burden of OM, its frequency and severity, varies among populations and risk groups and estimates of disease burden can be strongly influenced by definitions. In 1993 the World Health Organization (WHO) and the World Bank estimated that OM causes 51,000 deaths per year in children less than 5 years of age, mainly due to complications of chronic suppurative otitis media (CSOM).1 CSOM is estimated to affect between 65 and 330 million people, 60% of whom suffer significant hearing loss.2 The majority of this burden is in South East Asia, Western Pacific, Africa, and ethnic minorities. The WHO defines populations where the childhood prevalence of CSOM is ≥4% as having a public health emergency requiring immediate attention.3 Children with CSOM living in developing countries frequently require long-term (16 weeks) topical and/or systemic antibiotics to resolve the offensive discharge and improve hearing,4 some also require surgery to repair persistent perforation(s) in the tympanic membrane.5

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In developed countries, CSOM is now so rare that prevalence rates are not reported in the current literature.6 Most cases of CSOM in children are adverse events associated with surgical insertion of tympanostomy tubes.7 The major burden of OM is attributed to episodes of acute otitis media (AOM) and persistent otitis media with effusion (OME). Many children with AOM experience pain requiring oral analgesics. Many also require doctor visits and antibiotic therapy,8 particularly children less than 2 years of age with bilateral disease, and children with tympanic membrane perforation.9 Estimates of the incidence of AOM from longitudinal birth cohort studies range from 0.125 to 1.2 episodes per child year.10–12 For children prone to recurrent episodes of AOM, up to 7.3 episodes annually has been reported.13 In 60% of children with AOM, asymptomatic OME may persist for 3 months or more.6 The burden of OME is related to the associated conductive hearing loss that may affect language development as well as have social and educational outcomes. Management options for persistent OME with hearing loss include audiologic and medical interventions (antibiotic therapy and possibly surgery) to resolve the effusion and restore hearing.14,15

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Indigenous children (including those residing in industrialized countries) experience high rates of acute and chronic suppurative OM in addition to recurrent OM and persistent OME.16–19 Australian Aboriginal children living in remote communities have the highest published rates of CSOM and AOM with perforation.18 In 2001, a community-based survey that examined 709 (78%) of 914 eligible children between the age of 6 months and 2.5 years and living in 29 remote Aboriginal communities identified 24% as having perforated tympanic membranes (15% had CSOM, 2% dry perforation, and 7% AOM with perforation).18 An additional 26% had AOM (bulging tympanic membrane) without perforation and only 8% had bilaterally normal middle ears.

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In Australian Indigenous children, respiratory tract infections commence early in life and involve multiple bacterial species that result in recurrent episodes of AOM and progression to CSOM.20,21 Infants colonized with mixed pathogens, specifically those colonized with Streptococcus pneumoniae and Haemophilus influenzae, were at greater risk of OM [odds ratio (OR) = 33.6; 95% confidence interval (CI), 8–144] compared with those colonized with Moraxella catarrhalis alone (OR = 6.5; 95% CI, 2–29). Culture of ear discharge from acute perforations support a mixed bacterial etiology in this population; 57% cultured H. influenzae, 34% S. pneumoniae, and 21% cultured both pathogens (Table 1)22



A vicious circle of inflammation was hypothesized by Cole to explain the pathogenesis of chronic suppurative lung disease in adults with bronchiectasis.23 We believe that an extension of this model also explains the high rates of OM and other respiratory infections such as bronchiectasis in Aboriginal children.24,25 Dense and diverse bacterial nasopharyngeal colonization causes neutrophilic infiltration, tissue damage, increased mucus secretion, decreased mucociliary clearance, and leads to chronic suppurative lung disease in adults.23 However in the infant these events may also lead to CSOM and persistent nasal discharge. The persistent nasal discharge perpetuates the vicious circle, particularly where there is poor hygiene and overcrowding, by increasing opportunities for transmission among young infants. This includes transmission via hand contamination (in a community-based survey, 40% of children were found to have pneumococcal hand contamination).26 High rates of transmission events result in an accumulation of strains at a rate greater than can be cleared by the infant immune response or by damaged mucosa, and the vicious circle is repeated. For the middle ear, the high density of organisms and damaged mucosa are likely risk factors for failed therapy, recurrent AOM, and progression to perforation and CSOM. A role for respiratory viruses in AOM or failed therapy in these populations has not been described.

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Antibiotics for Prevention/Treatment of AOM


A meta-analysis of long-term antibiotic therapy found modest benefits in the prevention of AOM [Relative Risk (RR) = 0.62; 95% CI, 0.52–0.75] or AOM episodes [Incidence Rate Ratio (IRR) = 0.48; 95% CI, 0.37–0.62].13 Few randomized controlled trials of prolonged antibiotic therapy have been conducted in high-risk populations (rate of CSOM >4%); however, in a subgroup analysis the benefit of long-term antibiotics in preventing perforation in a high-risk population17 was substantial (RR = 0.61; 95% CI, 0.44–0.84; IRR = 0.52; 95% CI, 0.39–0.70) for preventing AOM in the subgroup of studies conducted primarily in the United State and Europe (RR = 0.62; 95% CI, 0.51–0.76; IRR = 0.51; 95% CI, 0.30–0.87).13

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Evidence from systematic reviews shows minimal benefit of antibiotics over placebo for pain associated with AOM at 2 to 7 days; antibiotic use was associated with an absolute reduction of 7% (95% CI, 4–10), (OR = 0.57; 95% CI, 0.45–0.73).8 Two studies reported perforation rates and these occurred in 7% of controls and in 4% of children receiving antibiotics (OR = 0.51; 95% CI, 0.2–1.3).8 A subsequent analysis of individual patient data from several of the studies in this meta-analysis and several new trials permitted secondary analysis to identify subgroups of children with CSOM most likely to benefit. In children younger than 2 years of age with bilateral AOM, 55% of controls and 30% on antibiotics still had pain, fever, or both at 3 to 7 days. The risk difference between these groups was 25% (95% CI, −36 to −14), resulting in a number-needed-to-treat (NNT) of 4 children. In children with otorrhoea, the risk difference and NNT, respectively, were −36% (95% CI, −53 to −19) and 3, whereas in children without otorrhoea the equivalent values were −14% (95% CI, −23 to −5) and 8.9

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Vaccines for Prevention of AOM

Pneumococcal Polysaccharide Vaccine (PPV: 8- or 14-Valent).

In the Cochrane systematic review of vaccines for preventing OM, the overall pooled rate ratio for PPV vaccination in prevention of AOM in the group of healthy children (no previous documented AOM episodes) was 0.92 (95% CI, 0.85 to 0.99).27 AOM episodes due to vaccine types (3 studies) was not significantly reduced (RR = 0.72. 95% CI, 0.43–1.21). The rate ratio in children younger than 24 months of age was 0.93 (95% CI, 0.83–1.05) and the rate ratio was 0.78 (95% CI, 0.63–0.97) for children older than 24 months. There was a significant reduction in AOM episodes in vaccinated children with previous AOM episodes (RR = 0.8; 95% CI, 0.69–0.93). Subgroup analysis shows a pooled rate ratio in the younger age group of 0.85 (95% CI, 0.74–0.98). The RR in the older age group was 0.74 (95% CI, 0.62–0.90).

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Pneumococcal Conjugate Vaccine (PCV).

Two randomized controlled trials (RCT) of infant schedules of 7-valent PCV were reported before licensure in the United States.12,28 Efficacy of PCV for prevention of vaccine serotype pneumococcal OM was 54% (95% CI, 41–64) in the FinOM RCT.12 Serotype replacement reduced efficacy for all serotype pneumococcal OM to 34% (95% CI, 21–45). Overall efficacy for clinical AOM was only 6% (95% CI, −6 to 16). The FinOM study also reported a nonsignificant increase in culture-confirmed H. influenzae AOM episodes (VE = −11%; 95% CI, −34 to 8). In the Northern California Kaiser Permanente study, per protocol efficacy for OM against visits, episodes, frequent otitis, and ventilatory tube placement was 8.9% (95% CI, 6–12), 7.0% (4–10), 9.3% (3–15), and 20.1% (2–35), respectively, with P < 0.04 for all. In the analysis of spontaneously draining ears, serotype-specific effectiveness was 66.7% (based on a relatively small number of specimens).28

The authors of the Cochrane Systematic Review concluded that the effects of PPV and PCV on the prevention of AOM are minimal. Irrespective of age, PPV would prevent 10% and PCV would prevent 8% of the AOM episodes, respectively.27 Approximately 32 children should be vaccinated with PPV or PCV to prevent 1 child from having an AOM episode during 1 year. To prevent 1 child younger than 24 months from having an AOM episode during 1 year, around 57 children should be vaccinated with PPV. PCV seemed a bit more effective compared with PPV—around 33 children need to be vaccinated with PCV to prevent 1 child from having AOM within a period of 1 year. Administering these vaccines on a large scale to prevent AOM cannot be recommended based on the currently available results.

An ecologic evaluation of PCV for prevention of OM in Australian Aboriginal children compared OM prevalence before and after a universal PCV program. In comparison with the 2001 data quoted above,18 in 2003, of 644 well children from 29 communities, 98% of whom had received 2 doses of pneumococcal conjugate vaccine, no significant reductions were found. An average of 21% had perforations (16% CSOM, 4% AOM with perforation, and 1% dry perforation), 24% had AOM without perforation, and a further 29% had OME. Bilateral normal ears were diagnosed in only 12% children. The microbiologic assessment supports the view that clinical failure in PCV-vaccinated children is most likely due to multiplicity of bacterial pathogens involved in AOM with perforation (AOMwiP), and to serotype replacement in pneumococcal AOMwiP. H. influenzae remains the major pathogen in AOMwiP (Table 1).22

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In high-risk populations where the childhood rate of CSOM is greater than 4% it is valuable to be able to identify those children at greatest risk of perforation. In community-based screening, around 20% to 30% of Australian Aboriginal children have bulging eardrums.29 Only 10% have typical symptoms that define AOM in low-risk populations (sudden onset of middle ear effusion with pain or redness).30 The value of bulging as a predictor of AOM has been confirmed in several high-quality studies but has not been emphasized in the AAP and AAFP guidelines.31 The implications of withholding antibiotic therapy in children with asymptomatic bulging ear drums have also not been evaluated in high-quality studies. However, our data from a randomized controlled trial of short-term antibiotics for AOM (bulging or perforated tympanic membrane) in a high-risk population indicated that AOM persists in around 50% of children.29 Guidelines for management of AOM in Indigenous children therefore define AOM as middle ear effusion with either bulging of the tympanic membrane, recent discharge, ear pain, or redness.32 There is no option to withhold antibiotics in an Aboriginal child with AOM, and for children with AOM with perforation, longer courses of antibiotics are recommended.

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The burden of respiratory disease is extremely high in Indigenous children. Bacterial colonization within weeks of birth and persistent exposure to multiple pathogenic species and strains are the greatest predictors of persistent and progressive disease. AOM does not resolve spontaneously if untreated, and may progress to perforation and CSOM in 25% of children. Long-term antibiotics are beneficial but are difficult for families, and antibiotic resistance may be a problem. Currently licensed vaccines have not had much impact on rates of OM. Although conjugate vaccines seem to prevent vaccine serotype-specific OM and carriage, replacement with nonvaccine serotypes negates much of the benefits. Vaccines that reduce infection to both S. pneumoniae and H. influenzae will be needed to substantially reduce the burden of disease in Indigenous children.10

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