Pediatr Infect Dis J, 2000;19:S316 Copyright 2000 by Lippincott Williams & Wilkins, Inc.

Vol. 19, No. 5 Printed in U.S.A.

Clinical epidemiology of otitis media

KATHLEEN A. DALY, PHD AND G. SCOTT GIEBINK, MD

The impact of otitis media (OM) on public health is considerable. OM is the most frequently diagnosed childhood disease in the United States. Between 1993 and 1995 OM was the most common diagnosis during office visits among 1- to 4-year-olds.1 OM constituted 18% of physician visits, compared with 14% of visits for well child care, 11% of visits for upper respiratory infection, 8% of visits for injury and 5% of visits for sore throat and tonsillitis. Thirty percent of children younger than 24 months in a large managed care organization were treated with tympanostomy tubes in 1994,2 and cost of OM treatment in the United States was estimated at $3.8 billion in 1995.3 Additionally OM was one of the most common reasons for deferral of diphtheria, tetanus, pertussis, polio, measles, mumps and rubella vaccines among inner city Baltimore children,4 which would increase their susceptibility to these vaccine-preventable diseases.
INCIDENCE, PREVALENCE, NATURAL HISTORY

Recent large prospective studies in the United States have investigated cumulative incidence of OM, using active surveillance and frequent examination. These studies reveal that at least 90% of children have one or more bouts of symptomatic or asymptomatic middle ear effusion (MEE) by the age of 2 years.5, 6 Peak age-specific incidence in the United States occurs in the first 2 years of life, typically between 6 and 18 months. In European countries, however, children enter child care later, which may delay peak incidence and the cumulative burden of OM (i.e. first OM episode is delayed and recurrent OM correspondingly reduced). Some studies have shown a bimodal distribution, with peak incidence at 1 to 2 years of age and again at 5 years, the latter age corresponding to school entry. About one-half of infants in the United States experience their first OM episode by 6 months of age, and early OM onset is associated with later recurrent OM and chronic otitis media with effusion (OME). The young infants developing immune system coupled with age-related differences in Eustachian tube anatomy
From the Otitis Media Research Center (KAD) and the Departments of Otolaryngology (KAD, GSG) and Pediatrics (GSG), University of Minnesota School of Medicine, Minneapolis, MN. Key words: Epidemiology, genetics, otitis media, prevalence. Address for reprints: Dr. Kathleen Daly, Otitis Media Research Center, Box 396 UMHC, 420 Delaware Street SE, Minneapolis, MN 55455. Fax 612-625-2101; E-mail dalyx002@tc.umn.edu.

and physiology make them particularly vulnerable to respiratory tract infection and OM. These characteristics increase susceptibility to respiratory pathogens and obstruct drainage of effusion formed during middle ear inflammation that accompanies an OM episode. Added to these liabilities, early exposures to environmental factors (e.g. child care attendance, respiratory viruses, parental smoking) also contribute to early and more frequent OM. Prevalence studies typically document the presence of OME using a variety of methods (i.e. tympanometry, otoscopy, myringotomy and audiometry), and rates vary widely by study. Nevertheless researchers have established that within a study population, OME prevalence declines with age, and rates are higher in the fall and winter than in the spring and summer. The ranges of reported age-specific OME prevalence rates were as follows: children 2 years of age, 6 to 11%; 2to 4-year-olds, 20 to 39%; 5- to 8-year-olds, 1 to 28%. Inuit children exhibited rates 20%7 and school age children (5 to 18 years) rates of 1 to 12%.8 Studies that calculated prevalence rates using ears rather than children were not included in these ranges because they underestimate the number of children affected. Differences in age-specific prevalence and incidence rates among studies can be due to a number of factors, including dissimilarities in study groups that affect OM susceptibility (e.g. race or ethnicity, risk factor status, season) or the likelihood of OM diagnosis (e.g. availability and use of health care, diagnostic methods and disease definitions, examination frequency). Prospective studies and randomized antibiotic trials provide insight into the natural history of OM resolution. Among children with OM, about two-thirds resolve their MEE within 1 month after the onset of OM, irrespective of treatment, and 90% resolve it in within 3 months.8 Younger children are more likely to have persistent effusion than older children; during the first 2 years of life mean proportion of time with MEE is 20%.
TRENDS OVER TIME

Rates of tympanostomy tube insertion appear to have increased 4-fold between 1970 and 1990.9 Practice patterns changed substantially during this time period as well, with tube insertions currently being performed predominantly in free-standing surgery centers and infrequently in hospitals. Comparison of tube rates S31

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performed in hospitals during this time would vastly underestimate the true tube rate. Therefore two sources of national data, one on hospital discharge diagnoses and another on ambulatory surgery diagnoses, were used for this comparison. Studies from Finland and the United States have reported increasing incidence of acute OM and recurrent OM; both studies also reported an increase in group child care during the study period.10, 11 Although increased OM incidence would be consistent with the observed increased attendance in group child care, changes in rates of breast-feeding and parental smoking are more complicated. Rates of breast-feeding at 6 months peaked in the United States at 25% in 1982 (up from 5% in 1971), declined to 18% in 1989 and then rose to 22% in 1995.12 Smoking rates for 20- to 44-yearolds have actually declined since 1974, with male rates dropping more rapidly than female rates.13 Receiving a diagnosis of OM depends on a number of variables, for example, diagnostic criteria, parent and physician awareness of OM and its risk factors and access to and use of health care. Changes in factors that contribute to the likelihood of OM diagnosis or ascertainment may have occurred over the same time period, resulting in an apparent increase in OM incidence. Demographic factors. Difficulties arise when comparing OM rates from studies of a homogenous group to make judgments about differences in OM susceptibility by race or ethnicity. Variability in study design, methodology or other population characteristics (e.g. socioeconomic status, risk factor profiles) may contribute to differences in OM rates that should not be attributed to ethnicity. Previous clinic-based research and survey data from national samples using parental report of childrens OM history revealed that African-American children were less likely to experience acute and recurrent OM or OME than white children.14, 15 However, Pittsburgh researchers using passive and active surveillance, monthly study visits and objective diagnostic criteria among biracial study populations demonstrated comparable rates of acute OM, MEE and the proportion of time with MEE in African-American and white children during the first 2 years of life and a strong inverse association between OME duration and socioeconomic status controlling for race.5, 16 Also, a national population-based study of school age children reported similar rates of OME for whites and AfricanAmericans, whereas Hispanics experienced higher OME prevalence.17 Inuit, Native American and Native Alaskan children have considerably higher rates of chronic OM than rates reported for similarly aged, predominantly white populations, although only one study included more than one ethnic group.7 In contrast the few longitudinal studies of Native American or Alaskan Native

children in early life describe OM incidence rates similar to those of white and African-American children. Young age clearly increases the risk of OM and OME, a finding established by a preponderance of evidence. Numerous studies have reported that male children are at higher risk of OM than female children, but several others have found no male-female disparity in rates. Socioeconomic status encompasses many independent factors that affect both the risk of OM and the likelihood of OM ascertainment. These include accessibility of medical care, race (often linked to social class), prevalence of risk factors (bottle-feeding, parental smoking), exposure to viruses and bacteria implicated in OM at child care or in crowded living conditions. The complexity of socioeconomic status and failure to adequately control for it in risk factor studies most likely accounts for contradictory findings about the association between socioeconomic status and OM risk. Additionally in studies using passive surveillance, middle and high income groups may appear to have higher OM rates than lower income groups because use of health care increases the likelihood of having OM ascertained. Environmental factors. Child care attendance and exposure to other young children (including siblings) has been established by numerous researchers and confirmed with metaanalysis as one of the major risk factors for OM, recurrent OM, OME and tympanostomy tubes. According to one metaanalysis, child care outside the home conferred a 2.5-fold risk of OM.18 A critical review of studies investigating child care and OM reported odds ratios of 1.1 to 2.6 for family vs. home care and 1.6 to 4.0 for center care vs. home care.19 Child care brings many children together in close contact, increasing the risk of both respiratory tract infection and OM. Several characteristics of the child care experience are related to increased exposure to other children and provide additional risk. These include center care, number of children in the setting or with whom the child has regular contact, hours spent in child care, age at entry, use of center care for the first placement, changes in care settings and having siblings in child care (this has been reported from Norway, where in contrast to the United States, infants do not enter child care until they are nearly 12 months old). However, recent studies have shown that among children followed prospectively or studied crosssectionally in child care centers, rates of OM and respiratory disease diminish with age, with older preschoolers appearing to be less prone to respiratory infections and concomitant episodes of OM. Presumably decreasing OM susceptibility with increasing age even among children in center care occurs because of maturing immune systems accompanied by ameliorat-

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ing changes in the angle and width of the Eustachian tube, which reduces the effects of viral and bacterial infections on the Eustachian tube and middle ear. Infant carriage of bacterial and viral pathogens implicated in OM and upper respiratory tract infection begins in the first few months of life. These pathogens can infect (or colonize) a child, and they are easily spread to others in the child care environment. Proposed mechanisms of viral action include injury to the middle ear and Eustachian tube epithelial cells, enhanced bacterial adhesion to these cells, lessening of middle ear mucociliary clearance, deleterious effects on cellular immune function and phagocytosis, tubal dysfunction resulting in negative pressure and serous transudate in the middle ear (which is an excellent growth medium for invading bacteria) and reduced antibiotic distribution from plasma to the inflamed middle ear. Although those in child care are more likely than other children to acquire active respiratory infections, they are also at higher risk of bacterial and viral colonization of the nasopharynx, which independently increases their OM risk. Scores of researchers have studied the role of infant feeding in OM. Many of these have reported that breast-feeding is protective, but recent studies have found protective effects only for exclusive breastfeeding lasting for 3 to 6 months. A metaanalysis of risk factor studies reported a 13% reduction in OM associated with breast-feeding of this duration.18 The effect of breast-feeding on OM has been reported to persist 4 to 12 months after breast-feeding cessation, perhaps because it delays the onset of the first OM episode and, thereby, reduces the frequency of OM recurrence. In contrast numerous investigators have failed to find an association between breast-feeding and OM or recurrent OM. Breast-feeding is a complex behavioral variable, which cannot be adequately described with terms such as breast-feeding or bottlefeeding. Researchers classification of infant feeding should include description of exclusivity of breast (or formula) feeding, duration of each specific feeding practice (exclusive breast, exclusive formula, combination feeding) and timing of introduction of supplemental foods.20 Another potential design problem is failure to adequately control for smoking and social class. Both are inversely related to breast-feeding but positively related to OM. In addition detection bias may exist if formula-feeding mothers are more likely than breastfeeding mothers to seek medical care for an ill child, thus increasing the likelihood of OM ascertainment.20 If breast-feeding reduces OM incidence and prevalence, several alternative explanations exist for its benefit. Lying flat during bottle feeding could cause milk to reflux into the middle ear, as first described by Duncan21 in 1960. A more recent study demonstrated

that among bottle-fed infants, 60% fed supine and 15% fed in the upright position had abnormal tympanograms suggestive of MEE after feeding.22 Alternatively components of breast milk have antimicrobial and immunomodulating properties that could prevent middle ear infections during and subsequent to breastfeeding. However, evidence about specific protective mechanisms is lacking. One study showed that exclusive breast-feeding reduced nasopharyngeal colonization with the three major OM pathogens, Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, at 6 months of age, although others have reported no effect of breast-feeding duration or exclusivity on colonization with H. influenzae. Breastfeeding has not been shown to reduce adherence of H. influenzae to respiratory epithelium, and activity of breast milk pneumococcal antibodies was not correlated with colonization or prevention of acute OM. Like breast-feeding, both positive and negative studies have been published on the role of exposure to passive smoke and childhood OM. Several studies have shown a dose-response relationship or increased OM risk only with heavy smoking. Two metaanalyses reported relative risks associated with exposure to passive smoke of 1.2 to 1.7, with an estimated 350 000 to 2 200 000 cases of middle ear disease attributable to this exposure annually in the United States.18, 23 A possible explanation for discrepancies in studies investigating passive smoke and OM is assessment of childs exposure, which is usually determined by maternal report of parents current smoking status and number of cigarettes smoked per day. Other important determinants of actual exposure to passive smoke include parents proximity to child when smoking, childs regular exposure to other smokers and time away from smoking parents (e.g. child care). Furthermore smoking parents may understate the amount they smoke or deny that they are smokers. Therefore quantification of a biomarker for smoke exposure is desirable to assess the childs actual degree of exposure. Studies in which cotinine have been assayed in the childs blood, saliva or urine have demonstrated a significant relationship between the level of this nicotine metabolite and OM risk. Probable mechanisms of the link between passive smoke exposure and childhood OM include inflammation of the mucosal surfaces of the nasopharynx, Eustachian tube and middle ear, rendering them more vulnerable to viral and bacterial infection; goblet cell hyperplasia, resulting in mucoid MEE, which is difficult to clear because it is often accompanied by impaired mucociliary clearance and Eustachian tube obstruction; inflammation of the respiratory tract airways, which increases susceptibility to respiratory infection, an important antecedent of OM; and greater exposure to respiratory infections, which are more

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common among smoking parents who then pass them on to their children. Genetics. Research has demonstrated the familial clustering of OM, and data are emerging on the role of genes in OM susceptibility. Sibling, maternal and paternal OM history has all been shown to be independently related to a childs OM risk. Shared OM history among siblings may be the result of inherited susceptibility and/or exposure to the same environmental factors and cultural practices. But when both parent and child develop OM, the likelihood of shared environmental exposure as the causative factor is not persuasive because parent and child reside in different environments during early childhood, the period of highest risk. To disentangle the role of heredity and environment, recent twin studies have examined the heritability of recurrent OM in 18- to 25-year-olds and total time with MEE in the first 2 years of life. Heritabilities of 72 to 75% were reported, with variability depending on gender and zygosity of the twin pairs.24, 25 Given the large estimate of heritability and the likelihood that heritability is multigenic, the next logical step is to identify genes linked to OM susceptibility. Knowledge of specific genes involved in OM would provide new insights into pathogenesis. A disease entity may arise from different etiologic pathways (genes at one locus or more, environmental factors or interaction of genes and environment). Subgrouping individuals based on molecular characteristics could elucidate known mechanisms of causation and lead to the discovery of previously unknown mechanisms, suggesting new avenues of treatment. Knowledge of a childs genetic susceptibility would impart more specific, DNA-based estimates of a childs risk to parents (a considerable improvement over knowledge of family history). It could also lead to individualized treatment strategies. Population-based studies would clarify the impact of susceptibility genes on disease burden and allow development and targeting of appropriate prevention activities, for example, eliminating environmental triggers and providing more aggressive surveillance for genetic susceptibles to prevent complications earlier in disease progression. Prenatal and perinatal factors. Because OM has its highest incidence in the first few years of life, it is logical to investigate risk factors from the prenatal and perinatal periods. A few studies have shown that lower birth weight and prematurity increased OM risk, although several others have reported no relationship between birth weight, gestational age and OM. However, more recent studies with large numbers of infants with very low birth weight, very preterm birth or intrauterine growth retardation have shown these chil-

dren to be at higher risk for OME and recurrent OM.26 28 Our recent study investigating the role of prenatal risk factors for early OM onset demonstrated a significant relationship between low levels of passively transferred maternal pneumococcal antibodies measured in cord blood and early OM.29 However, no associations were found among maternal prenatal diet, dietary supplements, use of drugs, alcohol, medications and symptoms and illnesses during the last trimester and early OM onset.30
CLINICAL IMPLICATIONS OF OM EPIDEMIOLOGY

The epidemiologic information on OM gathered to date has led to important avenues for fruitful investigation. Identification of the importance of OM onset in the first few months of life as a strong determinant of subsequent recurrent OM suggested environmental interventions (delayed or small group child care, breast-feeding advocacy) and immunologic strategies (maternal immunization against common infant OM pathogens). Identification of genetic determinants of OM susceptibility will yield a quantum leap in OM prevention through early detection of at risk infants. Racial and socioeconomic factors remain tightly intertwined, and discriminating one from the other factor as OM determinants has been difficult. Clearly respiratory viral infection remains one of the strongest infant and early childhood OM determinants, giving an incentive to develop immunoprophylaxis against these diseases. It is time to expand the clinicians use of this epidemiologic information in patient care while awaiting randomized trials to measure risk factor reduction on decreased OM incidence. In primary OM prevention, breast-feeding and small child care size should be promoted, household tobacco smoking should be discouraged and cleft (and submucous) palate should be identified early in life. A sibling history of early infant or recurrent OM should be known early in life and should lead to careful ear examinations during the first year. Despite a great deal of progress in the development of vaccines to prevent OM, there has been little research on preventive strategies to reduce risk factors as a method of primary prevention. As the Clinical Practice Guideline for OME points out, no randomized intervention studies have been conducted to learn whether reducing traditional risk factors (bottlefeeding, passive smoke exposure, child care size and respiratory infections) would impact OM incidence. However, two recent randomized intervention studies showed that: children of parents who received advice to reduce pacifier use had lower OM rates than controls,31 and children in child care who were randomly assigned

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to use xylitol gum or syrup for 3 months had lower acute OM rates than placebo recipients.32 Many have advocated that physicians advise parents to control environmental risk factors, although the typical physician receives little training on effective strategies to counsel parents about risk factor reduction. In our recent population-based study in Minnesota, only 25% of mothers of 8- to 12-month-old infants received advice from a physician or nurse about OM prevention, and the presence of risk factors was not related to having received this advice.33 Carefully planned randomized prevention trials are needed. They should be designed to measure risk factor reduction as an intermediate measure of intervention success, with decreased OM incidence as the outcome. There is sufficient knowledge of secondary OM prevention strategies to promote these as well. With the rising prevalence of antibiotic-resistant middle ear bacterial pathogens, judicious use of antibiotics is warranted. In particular the use of antibiotic chemoprophylaxis for recurrent OM has only limited indications today given the marginal impact (15% reduction) of this preventive strategy on recurrent OM. The child who clears MEE between recurrent OM episodes, but has three or more episodes in 6 months might be considered for chemoprophylaxis. Polyvalent pneumococcal vaccine [PneumoVax 23 (Merck & Co.); PnuImmune 23 (Lederle Laboratories)] is immunogenic in children older than 24 months and is likely to reduce OM incidence after this age. New pneumococcal conjugate vaccines are likely to have an effect on both infant pneumococcal colonization and OM incidence at a younger age. Surgical intervention (tube insertion, adenoidectomy) is also accepted secondary OM prophylaxis, based on the epidemiologic linkage of abnormal Eustachian tube function with recurrent OM.
CONCLUSIONS

OM, with its peak incidence in the first 2 years of life, is the most commonly diagnosed pediatric disease. Identified host characteristics are useful in targeting high risk children, and well-defined environmental factors present potential avenues of primary prevention. Advances in understanding the genetics of OM will continue and will dramatically change OM management in the future. Vaccines currently being fieldtested offer promise for primary prevention, and strategies for risk factor reduction should be tested and implemented. These strategies are complementary and provide a well-balanced approach to the reduction of OM morbidity into the 21st century.
REFERENCES
1. Freid VM, Mukuc DM, Rooks RN. Ambulatory health care visits by children: principal diagnosis and place of visit. Vital Health Stat 1998;13:123.

2. Myer CM III, France A. Ventilation tube placement in a managed care population. Arch Otolaryngol Head Neck Surg 1997;123:226 8. 3. Gates GA. Cost-effectiveness considerations in otitis media treatment. Otolaryngol Head Neck Surg 1996;114:52530. 4. Holt E, Guyer B, Hughart N, et al. The contribution of missed opportunities to childhood underimmunization in Baltimore. Pediatrics 1996;97:474 80. 5. Paradise JL, Rockette HE, Colborn K, et al. Otitis media in 2253 Pittsburgh-area infants: prevalence and risk factors during the first two years of life. Pediatrics 1997;99:318 33. 6. Owen MJ, Baldwin CD, Swank PR, Pannu AK, Johnson DL, Howie VM. Relation of infant feeding practices, cigarette smoke exposure, and group child care to the onset and duration of otitis media with effusion in the first two years of life. J Pediatr 1993;123:70211. 7. Homoe P, Christensen RB, Bretlau P. Prevalence of otitis media in a survey of 591 unselected Greenlandic children. Int J Pediatr Otorhinolaryngol 1996;36:21530. 8. Daly K. Definition and epidemiology of otitis media with effusion. In: Roberts JE, Wallace I, Henderson F, eds. In: Otitis media, language, and learning in young children. Baltimore: Paul H. Brooks Publishing, 1997:3 41. 9. Daly KA, Hunter LL, Giebink GS. Chronic otitis media with effusion. Pediatr Rev 1999;20:8594. 10. Joki-Erkkila VP, Laippala P, Pukander J. Increase in paediatric acute otitis media diagnosed by primary care in two Finnish municipalities: 1994 5 versus 1978 9. Epidemiol Infect 1998;121:529 34. 11. Lanphear BP, Byrd RS, Auinger P, Hall CB. Increased prevalence of recurrent otitis media among children in the United States. Pediatrics 1997;99:E1. 12. Ryan AS. The resurgence of breastfeeding in the United States. Pediatrics 1997;99:E12. 13. Pechmann C, Dixon P, Layne N. An assessment of US and Canadian smoking reduction objectives for the year 2000. Am J Pub Health 1998;88:13627. 14. Shurin PA, Pelton SI, Donner A, Klein JO. Persistence of middle ear effusion after acute otitis media in children. N Engl J Med 1997;330:11213. 15. MacTurk RH, Hoffman HJ, Overpeck MD, Jackson E. Risk factors for frequent ear infections in US children: results from the Third National Health and Nutrition Examination Survey (NHAMES III). In: Abstracts of the Seventh International Symposium on Recent Advances in Otitis Media, Fort Lauderdale, FL, June 1 to 5, 1999, p. 228. 16. Casselbrant ML, Mandel EM, Kurs-Lasky M, et al. Otitis media in a population of black American and white American infants, 0 2 years of age. Int J Pediatr Otorhinolaryngol 1995;33:116. 17. Hoffman HJ, MacTurk RH, Gravel JS, Chiu MS, Cosgrove CM. Epidemiological risk factors for otitis media and hearing loss in school age children based on NHANES III, 1988 1994. In: Abstracts of the Seventh International Symposium on Recent Advances in Otitis Media, Fort Lauderdale, FL, June 1 to 5, 1999, p. 59. 18. Uhari M, Mantysaari K, Niemela M. A meta-analytic review of the risk factors for acute otitis media. Clin Infect Dis 1996;22:1079 83. 19. Rovers MM, Zielhuis GA, Ingels K, et al. Day-care and otitis media in young children: a critical overview. Eur J Pediatr 1999;158:1 6. 20. Bauchner H, Leventhal JM, Shapiro ED. Studies of breastfeeding and infections: how good is the evidence? JAMA 1996;256:88792. 21. Duncan RB. Positional otitis media. Arch Otolaryngol 1960; 72:454 63. 22. Tully SB, Bar-Halm Y, Bradley RL. Abnormal tympanography after supine bottle feeding. J Pediatr 1995;126:S10511. 23. DiFranza JR, Lew RA. Morbidity and mortality in children associated with the use of tobacco products by other people. Pediatrics 1996;97:560 8. 24. Kvaerner KJ, Tambs K, Harris JR, Magnus P. Distribution and heritability of recurrent ear infections. Ann Otol Rhinol

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Laryngol 1997;106:624 32. 25. Casselbrant ML, Mandel EM, Fall PA, et al. The heritability of otitis media: a twin and triplet study. JAMA 1999;282: 212530. 26. Engel J, Anteunis L, Volovics A, Hendriks J, Marres E. Prevalence rates of otitis media with effusion from 0 to 2 years of age: healthy-born versus high-risk-born infants. Int J Pediatr Otorhinolaryngol 1999;47:24351. 27. Nalluswami K, Ko CW, Hou JR, Hoffman HJ. Very low birth weight (VLBW) infants are at increased risk for frequent ear infections [Abstract]. Am J Epidemiol 1998;147:S16. 28. Kvaerner KJ, Tambs K, Harris JR, Magnus P. The relationship between otitis media and intrauterine growth: a co-twin study. Int J Pediatr Otorhinolaryngol 1996;37:21725. 29. Salazar JC, Daly KA, Giebink, et al. Low cord blood pneumococcal immunoglobulin G (IgG) antibodies predict early onset acute otitis media in infancy. Am J Epidemiol 1997;145: 1048 56. 30. Daly KA, Brown JE, Lindgren BR, et al. Epidemiology of otitis media onset by six months of age. Pediatrics 1999;103: 1158 66. 31. Uhari M, Niemela M, Pihakari O, Pokka T. Pacifier as a risk factor for acute otitis media. In: Abstracts of the Seventh International Symposium on Recent Advances in Otitis Media, Fort Lauderdale, FL, June 1 to 5, 1999, p. 229. 32. Uhari M, Kontiokari T, Niemela M. A novel use of xylitol sugar in preventing acute otitis media. Pediatrics 1998;102: 879 84. 33. Daly KA, Selvius RE, Lindgren B. Knowledge and attitudes about otitis media risk: implications for prevention. Pediatrics 1997;100:931 6.

recurrent OM. Therefore, if you can delay the first episode 3 to 6 months, the incidence of recurrent OM is dramatically reduced. Question: Why do you think that early OM predicts recurrent OM? Is there any information and what is the mechanism? Dr. Giebink: There are many hypotheses. All studies have shown that there is a very strong, independent risk for recurrent OM with early OM. Question: Is it not true that most OM occurs in the first year of life whether it recurs or not? Dr. Giebink: Most recurrent OM that occurs in the first 6 months goes on. The vast majority of cases are in the first 6 months of life. Studies have shown that if OM was diagnosed at the 2-month office visit, there was over a 50% chance of having three or more episodes before the first birthday vs. a 20% chance if OM was not present at the 2-month visit. Question: Concerning breast-feeding, why is it an effective prevention? Is it because of immunoglobulins in the breast milk? Dr. Giebink: That is a possibility, but other factors may be present. There is a lot of lactoferrin in milk and there are other nonimmunologic mechanisms that may have a role. Let me add that bottle feeding results in a negative pressure in the bottle. Measurements of that pressure plus the pressure in the pharynx suggest that babies struggle to suck the bottle. Also, sucking on pacifiers appears to be related to OM. The negative pressure adversely affects the Eustachian tube (also in supine vs. prone sleeping positions). Breast-feeding is always under positive pressure.

QUESTIONS/ANSWERS

Question: In a study of 2000 children from shortly after birth to age 2 years, breast-feeding for 3 months had a carryover effect. Why does this occur? One theory is that the immune system is activated resulting in the long carryover protective effect. Dr. Giebink: My bias is that the carryover effect exists simply because early OM is reduced. Data indicate that early OM is the strongest determinant of