An outbreak of Plasmodium vivax malaria in Far North Queensland, 2002

OBJECTIVE: To describe an outbreak of Plasmodium vivax malaria in Far North Queensland in 2002. DESIGN: Epidemiological and entomological investigations; molecular analyses of the infecting parasites. MAIN OUTCOME MEASURES: Case characteristics, adult and larval mosquito counts at the outbreak location, haplotyping of parasites in blood samples from different cases determined through sequencing of AMA1 and MSP1 genes. RESULTS: A man with imported P. vivax malaria stayed at a camping ground 95 km north of Cairns in late September 2002. This led to an outbreak of P. vivax malaria in 10 adults who stayed at the camping ground in October. Large numbers of Anopheles farauti sensu lato larvae were present in stagnant pools in a creek at the camping ground, and many adult mosquitoes were collected nearby. Not only had most of the infected patients been exposed to mosquitoes at night, they were also less likely than other campers to have used insect repellents appropriately (odds ratio, 0.01; P < 0.001). Two different haplotypes of P. vivax, only one of which was detected in the imported case, were involved in the outbreak. CONCLUSIONS: Although local transmission of malaria is rare in Far North Queensland, the risk is probably higher in the dry season (September to December). Campers need to be aware of the increased risk of mosquito-borne diseases. Sexual recombination of multiple gametocytes in mosquitoes infected by the imported case may have resulted in the two haplotypes of P. vivax involved in the outbreak.     

Invasive pneumococcal disease in Indigenous people in north Queensland, 1999-2004

OBJECTIVE: To describe the epidemiology of invasive pneumococcal disease (IPD), and the impact of pneumococcal vaccines on IPD, in Indigenous people in north Queensland. SETTING: North Queensland, 1999-2004; there are about 53 750 Indigenous people in the region, including nearly 6900 children < 5 years and nearly 5650 adults > or = 50 years. MAIN OUTCOME MEASURES: Incidences of IPD in Indigenous children and in Indigenous adults compared between the 3 years before and after the introduction of a 7-valent pneumococcal conjugate vaccine (7vPCV) (1999-2001 versus 2002-2004). RESULTS: Estimated annual incidence of IPD in Indigenous children < 5 years of age declined from 170 to 78 cases per 100 000 in the 3 years following the introduction of 7vPCV in 2001. The annual incidence of vaccine-preventable IPD in Indigenous adults had declined by 86% since a 23-valent pneumococcal polysaccharide vaccine (23vPPV) was introduced to the region in 1996, to 15 cases per 100 000 (95% CI, 8-25) in 2002-2004. CONCLUSION: Although there was a rapid decline in IPD in young Indigenous children, it is unlikely that the incidence will fall much further with the current 7-valent vaccine. There was a suggestion that vaccinating Indigenous children indirectly protected those aged 5-14 years and Indigenous adults > or =15 years of age. Incidence of IPD in Indigenous adults in 2002-2004 was the lowest on record in the region.     

The first year of a midwifery-led model of care in Far North Queensland

OBJECTIVE: To describe a midwifery-led model of care in Far North Queensland and the outcomes obtained in its first year of operation. DESIGN, SETTING AND PARTICIPANTS: Prospective analysis of data for all women who were booked for antenatal care with the midwifery-led unit at Mareeba District Hospital (MDH) and who gave birth during its first year of operation, from 27 June 2005 to 30 June 2006. MAIN OUTCOME MEASURES: Number of women giving birth at MDH; antenatal, intrapartum and postpartum transfers to a higher-level referral centre (Cairns Base Hospital [CBH]); and labour and delivery outcomes. RESULTS: Of the 203 women who were booked for antenatal care at MDH and gave birth in the 12-month period, 170 were categorised as low risk and suitable to give birth at MDH. Of these, 147 (86%) did give birth at MDH, while 17 women (10%) had their care transferred antenatally to CBH, and six (4%) were transferred intrapartum. Of the 33 women categorised as high risk, 22 (67%) gave birth at CBH as planned, seven (21%) had elective caesarean sections performed by a general practitioner at MDH, and four (12%) presented to MDH in labour and gave birth there with no complications. Of the 158 women who gave birth at MDH, 146 (92%) had a spontaneous vertex delivery. CONCLUSION: Outcomes for the first year of operation of the midwifery-led model of care are consistent with a viable maternity unit, with delivery outcomes and transfer rates that compare favourably with other similar units in Australia.     

Type 2 diabetes in Indigenous and non-Indigenous children and adolescents in New South Wales

OBJECTIVE: To determine the incidence of type 2 diabetes mellitus (T2DM) in 2001-2006 in young people < 19 years and the characteristics of T2DM in the Indigenous group. DESIGN AND SETTING: Prospective population-based incidence study, New South Wales. PARTICIPANTS: Primary ascertainment was from the Australasian Paediatric Endocrine Group NSW Diabetes Register, with secondary ascertainment from the National Diabetes Register (Australian Institute of Health and Welfare). MAIN OUTCOME MEASURES: Incidence of T2DM in young people in NSW; incidence of T1DM and T2DM in Indigenous young people; characteristics at diagnosis. RESULTS: There were 128 incident cases of T2DM (62 boys, 66 girls) in the study period. The median age at diagnosis was 14.5 years (interquartile range, 13.0-16.4), and 90% were overweight or obese (body mass index > 85th percentile for age). Mean annual incidence was 2.5/100,000 person-years (95% CI, 2.1-3.0) in 10-18-year-olds. Of the ethnic groups represented, white Australian comprised 29%, Indigenous 22%, Asian 22%, North African/Middle Eastern 12% and Māori/Polynesian/Melanesian 10%. The incidence of T2DM was significantly higher in the Indigenous than the non-Indigenous group (incidence rate ratio, 6.1; 95% CI, 3.9-9.7; P<0.001), but incidence rates of T1DM were similar (15.5 v 21.4/100,000, respectively). CONCLUSIONS: T2DM accounts for 11% of incident cases of diabetes in 10-18-year-olds, and the majority are overweight or obese. The high rate among Indigenous Australian children supports screening for T2DM in this population.     

Invasive pneumococcal disease in Indigenous people in north Queensland: an update, 2005-2007

OBJECTIVE: To examine trends in invasive pneumococcal disease (IPD) in Indigenous people in north Queensland following the introduction of the 7-valent pneumococcal conjugate vaccine (7vPCV). DESIGN: Trends in IPD were compared over three 3-year periods: before the introduction of 7vPCV for Indigenous children (1999-2001), and two consecutive periods after its introduction (2002-2004 and 2005-2007). MAIN OUTCOME MEASURES: Incidences of IPD in Indigenous children and adults in 1999-2001 and 2005-2007; trends in IPD caused by 7vPCV and non-7vPCV serotypes; and trends in indirect protective effects and emergence of non-7vPCV serotype IPD. RESULTS: From 1999-2001 to 2005-2007, there was a 60% decline in IPD, with the virtual elimination of 7vPCV serotype IPD in young (< 5 years) Indigenous children. There is no evidence yet of an increase in non-7vPCV serotype IPD in these children. Although the annual incidence of IPD in Indigenous adults remained virtually unchanged, there was a 75% decline in 7vPCV serotype IPD in these adults (chi2(trend) = 11.65, P < 0.001). However, the incidence of IPD caused by non-7vPCV serotypes more than tripled in adults (chi2(trend) = 7.58, P = 0.006). Serotype 1 IPD has been prominent over the 9 years, but there is no evidence of a recent increase in serotype 19A IPD. CONCLUSIONS: Vaccinating Indigenous children with 7vPCV has protected Indigenous adults in north Queensland through an indirect "herd immunity" effect. However, this benefit has been offset by a recent increase in non-7vPCV IPD in Indigenous adults. Newer pneumococcal conjugate vaccines could prevent, both directly and indirectly, a considerable amount of the persisting IPD in Indigenous people in the region.     

Causes of inequality in life expectancy between Indigenous and non-Indigenous people in the Northern Territory, 1981-2000: a decomposition analysis

OBJECTIVE: To identify the causes of the gap in life expectancy between Indigenous and non-Indigenous populations of the Northern Territory and how the causes have evolved over time. DESIGN AND SETTING: Analysis of NT death data over four 5-year periods, 1 January 1981 to 31 December 2000 inclusive. A decomposition method using discrete approximations (Vaupel and Romo) was applied to abridged life tables for the Indigenous and non-Indigenous populations of the NT. MAIN OUTCOME MEASURES: Contribution of causes of death, grouped according to global burden of disease groups and categories, to the life expectancy gap. RESULTS: The gap between the life expectancy of Indigenous and non-Indigenous people in the NT did not appear to narrow over time, but there was a marked shift in the causes of the gap. In terms of disease groups, the contribution of communicable diseases, maternal, perinatal and nutritional conditions halved during the 20 years to 2000. Meanwhile, the contribution of non-communicable diseases and conditions increased markedly. The contribution of injuries remained static. In terms of disease categories, the contribution of infectious diseases, respiratory infections and respiratory diseases declined considerably; however, these gains were offset by significantly larger increases in the contribution of cardiovascular diseases and diabetes for Indigenous women and cardiovascular diseases, cancers and digestive diseases for Indigenous men. CONCLUSIONS: The main contributors to the gap in life expectancy between the Indigenous and non-Indigenous populations were non-communicable diseases and conditions, which are more prevalent in ageing populations. With the life expectancy of Indigenous people in the NT expected to improve, it is important that public health initiatives remain focused on preventing and managing chronic diseases.     

Health of Aboriginal and Torres Strait Islander children in remote Far North Queensland: findings of the Paediatric Outreach Service

AIM: To describe the pattern of disease and other health problems in children living in remote Far North Queensland (FNQ). DESIGN, SETTING AND PARTICIPANTS: Retrospective review of the FNQ Paediatric Outreach Service's Medical Director database for the period June 2001 to February 2006. Three subpopulations were compared: children from predominantly Aboriginal communities, predominantly Torres Strait Islander communities, and other communities. All children referred to the service during the study period were reviewed. MAIN OUTCOME MEASURES: Number of children seen and common diagnoses. RESULTS: 3562 children were referred during the study period, and a total of 3932 diagnoses were made; 56% of the paediatric population of the Aboriginal communities and 23% of the paediatric population of Torres Strait Islander communities were seen. Of 40 separate diseases/health problems reviewed, the three most common reasons for presentation were chronic suppurative otitis media, suspected child abuse and neglect, and failure to thrive. In the paediatric population of Aboriginal communities, the prevalence of fetal alcohol spectrum disorder was at least 15/1000 (1.5%), and in Torres Strait Islander children, rheumatic heart disease prevalence was at least 6/1000 (0.6%). Rheumatic fever rates were among the highest in Australia. CONCLUSION: Rates of preventable complex and chronic health problems in Aboriginal and Torres Strait Islander children in remote FNQ are alarmingly high. Areas requiring urgent public health intervention include alcohol-related conditions and rheumatic fever.     

Perinatal and postneonatal mortality among Indigenous and non-Indigenous infants born in Western Australia, 1980-1998

OBJECTIVE: To describe cause-specific perinatal and postneonatal mortality for Indigenous and non-Indigenous infants using a new classification system. DESIGN: Total population retrospective cohort study. PARTICIPANTS AND SETTING: All registered births in Western Australia of birthweight greater than 399 g from 1980 to 1998, inclusive. MAIN OUTCOME MEASURES: Rates and time trends for all births 1980-1998, and cause-specific rates for births 1980-1993 of fetal, neonatal and postneonatal mortality among Indigenous and non-indigenous infants, using a classification system designed for use in perinatal, postneonatal and childhood deaths. RESULTS: For Indigenous infants born 1980-1998, the mortality rate before the first birthday was 2.7 times (95% CI, 2.5-2.9 times) that for non-Indigenous infants. Indigenous infants born 1980-1993 had a higher mortality rate in all cause-of-death categories. The highest relative risk was for deaths attributable to infection (8.1; 95% CI, 6.5-10.0) which occurred primarily in the postneonatal period; the source of the infection was less likely to be identified in Indigenous deaths. From 1980-1998, the rate of neonatal deaths decreased at a greater rate for Indigenous than for non-Indigenous infants. However, while stillbirth and sudden infant death syndrome rates for non-Indigenous births fell, they remained static for Indigenous births. CONCLUSIONS: The new classification system, which considers the underlying rather than immediate cause of death, enables investigation of the causes of all deaths, from stillbirths to childhood. This system has highlighted the comparative importance of infection as a cause of death for Indigenous infants, particularly in the postneonatal period.     

Carriage of methicillin-resistant Staphylococcus aureus in a Queensland Indigenous community

OBJECTIVE: To determine the prevalence of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) carriage and infection among children living in an Indigenous community in Queensland. DESIGN, SETTING AND PARTICIPANTS: Swabs for culture of S. aureus were collected from the nose, throat and skin wounds of primary school children. MAIN OUTCOME MEASURES: MRSA carriage, antibiotic sensitivity, genotype, and presence of the virulence factor Panton-Valentine leukocidin (PVL); and epidemiological risk factors for MRSA carriage. RESULTS: 92 (59%) of 157 eligible children were included in the study. Twenty-seven (29%) carried S. aureus; 14 of these (15% of total) carried MRSA. MRSA was isolated from 29% of wound swabs, 8% of nose swabs, and 1% of throat swabs. Fourteen of 15 MRSA isolates were sensitive to all non-beta-lactam antibiotics tested. Eight children (9%) carried CA-MRSA clonal types: six carried the Queensland clone (ST93), and two carried the South West Pacific clone (ST30). All these isolates carried the virulence factor PVL. The remaining six children carried a hospital-associated MRSA strain (ST5), negative for PVL. CONCLUSIONS: We have identified a high prevalence of CA-MRSA carriage in school children from a Queensland Indigenous community. In this setting, antibiotics with activity against CA-MRSA should be considered for empiric therapy of suspected staphylococcal infection. Larger community-based studies are needed to improve our understanding of the epidemiology of CA-MRSA, and to assist in the development of therapeutic guidelines for this important infection.     

Hospitalisation for head injury due to assault among Indigenous and non-Indigenous Australians, July 1999--June 2005

OBJECTIVE: To describe rates of hospitalisation for head injury due to assault among Indigenous and non-Indigenous Australians. DESIGN, SETTING AND PARTICIPANTS: Secondary analysis of routinely collected hospital morbidity data for 42,874 inpatients at public and private hospitals in Queensland, Western Australia, South Australia and the Northern Territory for the 6-year period 1 July 1999--30 June 2005. MAIN OUTCOME MEASURES: Rates per 100,000 population of head injury due to assault by Indigenous status, age, sex and location of residence. RESULTS: The overall rate of head injury due to assault was 60.4 per 100,000 population (95% CI, 59.8-60.9). The rate among the Indigenous population was 854.8 per 100,000 (95% CI, 841.0-868.9), 21 times that among the non-Indigenous population (40.7 per 100,000; 95% CI, 40.2-41.2). Most Indigenous (88%) and non-Indigenous (83%) victims of head injury due to assault were aged between 15 and 44 years. The peak incidence among the Indigenous population was in the 30-34-year age group, whereas that among the non-Indigenous population was in the 20-24-year age group. Indigenous females experienced 69 times the injury rate experienced by non-Indigenous females. CONCLUSIONS: Indigenous people, particularly women, were disproportionately represented among those hospitalised for head injury due to assault. Head injury imposes a substantial burden of care on individuals and communities. Along with the costs of treating head injury, these are good reasons to strengthen efforts to prevent head injury generally, with special attention to high-risk population segments.     

Survival of Indigenous and non-Indigenous Queenslanders after a diagnosis of lung cancer: a matched cohort study

OBJECTIVE: To compare survival of Indigenous and non-Indigenous lung cancer patients and to investigate any corresponding differences in stage, treatment and comorbidities. DESIGN AND SETTING: Cohort study of 158 Indigenous and 152 non-Indigenous patients (frequency-matched on age, sex and rurality) diagnosed with lung cancer between 1996 and 2002 and treated in Queensland public hospitals. MAIN OUTCOME MEASURES: Survival after diagnosis of lung cancer; effects of stage at diagnosis, treatment, comorbidities and histological subtype on lung cancer-specific survival. RESULTS: Survival of Indigenous lung cancer patients was significantly lower than that of non-Indigenous patients (median survival, 4.3 v 10.3 months; hazard ratio, 1.48; 95% CI, 1.14-1.92). Of 158 Indigenous patients, 72 (46%) received active treatment with chemotherapy, radiotherapy or surgery compared with 109 (72%) of the 152 non-Indigenous patients, and this treatment disparity remained after adjusting for histological subtype, stage at diagnosis, and comorbidities (adjusted risk ratio, 0.65; 95% CI, 0.53-0.73). The treatment disparity explained most of the survival deficit: the hazard ratio reduced to 1.10 (95% CI, 0.83-1.44) after inclusion of treatment variables in the proportional hazards survival model. The remaining survival deficit was explained by the higher prevalence of comorbidities among Indigenous cancer patients, mainly diabetes. CONCLUSION: Survival after a diagnosis of lung cancer is worse for Indigenous patients than for non-Indigenous patients, and differences in treatment between the two groups are mainly responsible.