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Summary of Hib among Indigenous people

Differences in the patterns of Hib infection observed among Indigenous and non-Indigenous children in the pre-vaccination era were clearly documented in total disease incidence, age distribution, clinical manifestations and risk factors for disease. The pattern since the implementation of the national vaccination strategy has been less well documented. It is clear that incidence rates, and consequent morbidity and mortality, have dropped dramatically in both non-Indigenous and Indigenous populations, but disease persists, albeit at lower levels.

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The pre-vaccination era

In the era preceding vaccination, Indigenous children, particularly those from rural areas, exhibited patterns of Hib infection similar to those documented in developing countries and among the most disadvantaged populations in developed countries [3, 11]. Meningitis and pneumonia were the most common manifestations, and epiglottitis was not reported among the Indigenous population [9, 11, 13]. Incidence estimates for Indigenous children from this period varied across geographic locations, but were consistently greater than those reported for non-Indigenous children [5, 11]. In central Australia, incidence rates were higher than those reported anywhere else in the world [12]. Disease was typically contracted before the age of one [5, 11] and there was a greater risk of mortality and long-term morbidity [12, 14].

In contrast, non-Indigenous children demonstrated the epidemiological pattern observed in other developed countries, typically presenting with meningitis or epiglottitis. About half the cases occurred in children over 18 months of age. The case fatality rate was low [7]. Estimates of the incidence of Hib disease among non-Indigenous Australians under 5 years of age from various parts of Australia typically ranged between 25 and 60 per 100,000 poplation [7, 11, 15, 16, 17].

Factors contributing to Hib disease among Indigenous children

The high incidence rates and poor outcomes observed among Indigenous children in the pre-vaccination era suggest that other risk factors (additional to those typically associated with Hib infection) contributed to the burden of Hib disease suffered by the Indigenous population [11]. There is evidence to suggest that the extremely high incidence of Hib disease observed among central Australian Aboriginal people prior to vaccination may have been due in part to their exposure to more virulent strains of Hib [9], or to genetic differences in susceptibility [5]. However, most of the factors that have influenced the risk of disease in Indigenous children have been associated with their poor social and environmental conditions [5].

Poor nutritional status is not uncommon among Indigenous children and may increase the risk of Hib infection . Low levels of breastfeeding among urban Indigenous populations are likely also to increase the risk. The poor living conditions frequently documented in Indigenous communities are considered ideal for the transmission of Hib, as they contribute to crowding and increase the risk of respiratory tract viruses that in turn facilitate infection with Hib. Other environmental conditions, such as exposure to woodsmoke, dust, and passive smoking, are thought also to compromise immunity and increase the susceptibility of Indigenous children to Hib infection [5]. Thus, a variety of factors may have contributed to the increased incidence of disease observed among Indigenous children in the pre-vaccination era. In those in whom disease did develop, mucosal damage and/or increased mucosal colonisation may have facilitated invasion into the blood, the resultant bacteraemia and symptomatic disease [2].

Evidence of Hib disease among Indigenous children

Numerous studies reported high incidence rates of Hib disease among Indigenous children in the years immediately preceding the introduction of Hib vaccination. Except for reports about Hib meningitis, there were few reports, however, about the full impact of invasive disease.

Incidence
Pre-vaccination incidence rates for Hib disease among Indigenous children varied between States and Territories. Estimates ranged from a complete absence of the disease among Indigenous people in the ACT [19] to 115 per 100,000 in Queensland [17], 225 per 100,000 in WA [15], 530 per 100,000 in the Northern Territory overall and 990 per 100,000 in central Australia [12]. The latter rate is higher than any reported internationally [9], and of an order of magnitude above and beyond that reported elsewhere in the nation [19].

Morbidity
Pneumonia, bacteraemia, and other forms of invasive Hib disease are all severe infections and may all require hospitalisation, but the higher incidence and serious outcomes associated with meningitis resulted in more detailed documentation of the short and long-term effects of this disease.

The short-term effects are exemplified in a study of bacterial meningitis among Indigenous children from the Northern Territory . The mean length of hospitalisation for Indigenous children was 15.5 days and significantly longer than the 9.9 days for non-Indigenous children [20]. The longer period of hospitalisation for Indigenous children could have been due to severity of illness, multiple diagnoses and/or subsequent complications [20]. A Western Australian study of the long-term effects of Hib meningitis demonstrated a three-fold increased risk of severe sequelae (defined as severe or profound intellectual and/or physical disability, such as cerebral palsy) among Indigenous children [14]. All cases of severe sequelae in Indigenous children occurred among those from the remote north and east of the State, so delays in transportation, diagnosis and/or treatment may have contributed to the poorer outcomes [14].

Mortality
The mortality associated with invasive Hib disease among Indigenous children was low compared to that attributed to many other causes, and case fatality rates were minimised by the availability of evacuation services and intensive care facilities [12]. Despite these services, mortality rates for Hib mortality was higher consistently for Indigenous children than for non-Indigenous children. In the Northern Territory, the case fatality rate of Hib meningitis in Indigenous children was 8.3% in the mid to late 1980s [12]. There were no deaths due to Hib meningitis among non-Indigenous children in the same period. Similar figures, ranging from 8.6% to 14%, were reported in a number of studies conducted in Western Australia [14, 15, 21]. All Indigenous case fatality rates were significantly greater than those reported for non-Indigenous children.

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The post-vaccination era

The medical and social importance of Hib infection generally, and within Indigenous populations particularly, resulted in the implementation in July 1993 of a fully-funded national infant program . Funding for a national 'catch-up' program targeting all children up to 5 years of age commenced in August 1993 [10, 15] Various studies conducted in the period following the introduction of Hib vaccines documented a marked decrease in the incidence of invasive Hib disease in Australian children [8, 15, 16, 18]. Both the Hib Case Reporting Scheme and the National Notifiable Diseases Surveillance System documented a fall of approximately 50% in the number of cases of invasive Hib disease reported in Australia between 1 July 1993 and 30 June1994 [8].

Evidence of Hib disease among Indigenous children

In Western Australia, information regarding the decline in invasive Hib disease has been derived from a population-based active surveillance system for non-Indigenous cases and a population-based, matched, case-control study for Indigenous children. Figures from 1994 demonstrated a rapid decline in the incidence of invasive Hib disease in both Indigenous and non-Indigenous children following the introduction of vaccination [15]. However, three cases of invasive Hib infection were reported in fully vaccinated Indigenous children and the study was unable to demonstrate that Hib vaccination conferred a statistically significant benefit for the Indigenous population. In contrast, not a single case of Hib meningitis was reported in Aboriginal or Torres Strait Islander children in far north Queensland between July 1993 and the end of 1994 [18]. In the Northern Territory, the incidence of invasive Hib disease in Indigenous children is reported to have dropped from 278 per 100,000 child-years in the pre-vaccination period (January 1989 to June 1993), to 37 per 100,000 child-years in the post-vaccination period (July 1993-December 1996) [16]. The relative risk of disease in Indigenous children following the introduction of vaccination, compared with the risk before vaccination, was calculated to be 0.13.

The persistence of Hib disease

Despite the rapid decrease in the number of reported Hib cases, nasopharyngeal carriage of Hib persists [22 cited in 23] and invasive disease continues to occur. Between July 1993 and June 1996, Australia-wide surveillance identified 412 cases of invasive disease due to Hib. Included were 18 deaths and 34 cases of vaccine failure (according to the Australian case definition of a vaccine failure) [24]. Ongoing surveillance is therefore necessary to evaluate the continuing efficacy of the Hib vaccination program. This applies to the Australian population as a whole. It may be particularly important for the Indigenous population, as evidence from the United States (US) confirms that Hib disease continues to occur, albeit at lower levels, in socioeconomically disadvantaged populations [6]. In the US, having a single parent mother and living in a crowded household remained independent risk factors for Hib disease regardless of vaccination status.

Additional prevention and control measures

Reduced numbers of Hib cases can clearly be attributed to the introduction of Hib vaccines, but the continued occurrence of cases will necessitate chemoprophylaxis under some circumstances. In the Kimberley, even in communities with high levels of immunisation, rifampicin is recommended for all household/family contacts of cases if any of the contacts are less than one year of age or if any of the contacts are aged between one and five years and are inadequately vaccinated [25].

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Non-type b Haemophilus influenzae

Prevention and control strategies for Hib have markedly reduced the incidence of invasive disease, but comprehensive measures are still warranted for non-type b H. influenzae infections. Although traditionally less common and less serious than Hib, these infections have been responsible for morbidity and mortality among children in Indigenous populations and in developing countries, and will continue to be a problem despite Hib vaccination. Australian studies have confirmed that non-type b H. influenzae infections were responsible for as much as 20% of invasive disease in Indigenous children in the period preceding vaccination [4, 12]. While encapsulated strains of H. influenzae other than type b do cause invasive disease, non-encapsulated strains are more likely to cause mucosal infections (such as conjunctivitis and otitis media) and respiratory infections (such as bronchitis) [1, 3]. These infections also cause considerable morbidity and may become secondarily invasive in immuno-compromised individuals [3]. Recent studies have reported particularly high carriage rates of non-encapsulated H. influenzae among Indigenous infants and children [23, 26].

Evidence of mucosal infections in the Indigenous population

Conjunctivitis and otitis media provide examples of the increased risk of H. influenzae mucosal infections in the Indigenous population. Of 39 cases of H. influenzae conjunctivitis that occurred during an outbreak in the Katherine region in 1991, 36 were Indigenous and a number were severe enough to warrant hospitalisation. Cases occurred throughout the Katherine region, but the outbreak was focused in an Indigenous community where it was apparently precipitated by overcrowding during a festival. Cases occurred most commonly in the 0-4 year age group, but all ages were affected. Symptoms resolved quickly following treatment with a single oral dose of amoxycillin and probenicid [27]. Unlike H. influenzae conjunctivitis, which occurs sporadically, otitis media is highly prevalent among Indigenous infants and children. Recent studies indicate that early, dense bacterial colonisation of the nasopharynx with multiple species of respiratory bacteria (including a predominance of non-encapsulated H. influenzae) contribute to the early onset, persistence and severity of otitis media in Indigenous children [23, 28, 29, 30].

Prevention and control measures

Further studies are required to fully elucidate the epidemiology of the various H. influenzae diseases, but control of non-type b H. influenzae will certainly depend on improvements in environmental, social and economic conditions. Less crowded living conditions, improved indoor air quality and improved hygiene are likely to reduce the risk of infection, as will strategies designed to promote infant growth and development and reduce the transmission of infectious diseases [5]. Hanna (1992) suggests that such strategies should include family planning services, optimal antenatal and obstetric care, promotion of breastfeeding, improved weaning and food preparation practices, growth monitoring, childhood immunisation, and frequent hand and face washing.

Such holistic primary prevention measures will be particularly important if, as has been documented elsewhere [31], H. influenzae develops resistance to such antimicrobial agents as ampicillin, rifampicin and tetracycline. Of added concern is the nasopharyngeal carriage of non-encapsulated H. influenzae isolates which are genetically similar to Hib, and the theoretical possibility of genetic exchange between Hib and non-encapsulated H. influenzae strains in Indigenous populations where the organism is highly endemic [23]. Such concerns demonstrate the relationship between Hib and other H. influenzae organisms and highlight the need for continued surveillance of Hib immunisation and H. influenzae carriage.

References
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Last updated: 28 August 2008