Communicable disease

Please select category from the dropdown list below.

Selected health conditions    Cardiovascular health    Cancer    Diabetes    Social and emotional wellbeing (including mental health)    Kidney health (renal disease)    Injury    Respiratory health    Eye health    Ear health    Oral health    Disability    Communicable disease

Communicable diseases

Communicable diseases of particular importance to Indigenous people include: tuberculosis, hepatitis (A, B, and C), sexually transmissible infections, HIV/AIDS, Haemophilus influenzae type b (Hib), pneumococcal disease, and meningococcal disease [1].

Communicable diseases can be caused by: bacteria (e.g. pertussis (whooping cough) and tuberculosis); viruses (e.g. influenza and HIV); fungi (e.g. tinea); or protozoan parasites (e.g. malaria) [2][3]. Communicable diseases also include infestation with larger parasites, such as head lice, as well as diseases which are spread through infectious particles, such as transmissible spongiform encephalopathies [3]. Risk factors for communicable diseases vary according to the type of disease [1]. Improvements to sanitation, and the increased use of vaccination and antibiotics (for bacterial infections), have markedly reduced some infectious diseases in Australia [4].

Information regarding specific communicable diseases comes from a variety of sources, including individual studies and the state and territory notifiable disease collections. Data from state and territory collections are collected and published by the National Notifiable Disease Surveillance System (NNDSS), but Indigenous status is often not reported for large proportions of notifications. Information about some communicable diseases is analysed and published by specialised external agencies, including the Kirby Institute (formerly the National Centre in HIV Epidemiology and Clinical Research) for sexually transmissible infections, hepatitis and HIV/AIDS, and the National Centre for Immunisation Research and Surveillance for vaccine-preventable diseases.

Tuberculosis

Tuberculosis (TB) is primarily a lung infection caused by the inhalation of the bacterium Mycobacterium tuberculosis [5]. The bacterium can penetrate the lungs and start to multiply, potentially causing a variety of symptoms including: coughing; weight loss; loss of appetite; fever; chills; and the coughing up of blood or sputum. The main risk factors for TB are poverty, overcrowding, and malnutrition [6][7], all common in many Indigenous communities. Other risk factors also common among Indigenous people are diabetes mellitus, smoking, alcohol use, and advanced kidney disease [7]. Another risk factor for TB is HIV infection [8].

Extent of tuberculosis among Indigenous people

Of the 800 notifications of TB among Australian-born people in Australia in 2005-2009, 152 (19%) were identified as being Indigenous (Derived from [9][10][11][12]). Almost one-half (43%) of the new cases among Indigenous people were reported in the NT (65 cases), and around one-third (32%) in Qld (48 cases) (Table 26). Australia-wide, the crude notification rate in 2005-2009 was 5.8 cases per 100,000 population for Indigenous people; the crude notification rate was highest for the NT (20 cases per 100,000 population) (Derived from [13][9][10][11][12][14]). After age-adjustment, the notification rate for Indigenous people was 11.1 times that for Australian-born non-Indigenous people (Table 27) (Derived from [13][9][10][11][12][14]).24

The notification rate of TB was higher for Indigenous people than for Australian-born non-Indigenous people across all age-groups, with rate ratios being highest for the 35-44 years, 45-54 years and 55-64 years age-groups (Table 27) (Derived from [13][9][10][11][12][14]).

Table 26: Numbers of new cases and crude notification rates of tuberculosis among Indigenous people, by jurisdiction, Australia, 2005-2009

Jurisdiction	Number	Rate
Source: Derived from Roche, 2007 [9], Roche, 2008 [10], Barry, 2009 [11], Barry, 2012 [12], ABS, 2007 [14], ABS, 2009 [13]
Notes: Population figures are for 30 June 2007 (the mid-point of the five-year period, 2005-2009) Rates are crude incidence rates per 100,000 population
NSW	21	2.7
Vic	4	2.3
Qld	48	6.5
WA	6	1.7
SA	6	4.2
Tas	2	2.1
ACT	0	0.0
NT	65	20.0
Australia	152	5.8

Table 27: Numbers of new cases and notification rates of tuberculosis, by Indigenous status and age-group, and Indigenous:non-Indigenous rate ratios, Australia, 2005-2009

Age-group (years)	Indigenous		Non-Indigenous		Rate ratio
	Number	Rate	Number	Rate
Source: Derived from Roche, 2007 [9], Roche, 2008 [10], Barry, 2009 [11], Barry, 2012 [12], ABS, 2007 [14], ABS, 2009 [13]
Notes: Rates are per 100,000 population Any discrepancy between the figures shown for ‘All ages’ and the sum of the number for the specific age-groups is due to age not being stated in the notification Rate ratio is the Indigenous rate divided by the non-Indigenous rate The rate ratio for ‘All ages’ is the standardised notification ratio, which is the number of Indigenous cases reported divided by the number expected if the Indigenous population had the same age-specific rates as the non-Indigenous population
0-4	5	1.5	55	0.9	1.8
5-14	12	1.8	47	0.4	5.1
15-24	17	3.3	70	0.5	6.6
25-34	25	6.8	71	0.5	14
35-44	30	9.0	47	0.3	29
45-54	31	13.3	62	0.4	31
55-64	19	14.8	60	0.5	29
65+	13	15.8	236	1.7	9.2
All ages	152	5.8	648	0.6	11.1

Hepatitis

Hepatitis, an inflammation of the liver, can be caused by viral infections, alcohol or drug use, other toxins, or an attack by the body’s immune system on itself [15]. The viruses identified most frequently have been designated hepatitis A, B, and C (hepatitis types D through G have also been identified, but hepatitis F and G are not regarded as true hepatitis viruses). The following sections summarise information about hepatitis A, B, and C.

Hepatitis A

The hepatitis A virus (HAV) is an infection of the liver predominantly transmitted by the faecal-oral route, either through ingesting contaminated food or water or by direct contact with an infected person (including sexual contact, particularly between men) [16][17]. HAV is often asymptomatic among young children, but symptoms among older people may include fever, fatigue, nausea, diarrhoea, jaundice, and vomiting. Death due to HAV is very rare.

Of the 155 notifications of HAV for people living in WA, SA, and the NT in 2009-2011, three (1.9%) were identified as Indigenous (Derived from [13][18][19][20][21]). The crude notification rate of 0.6 per 100,000 for Indigenous people was less than the rate of 1.3 per 100,000 for non-Indigenous people.

It is likely that the lower levels of HAV infection among Indigenous people reflect the introduction in 2005 HAV vaccination into the national childhood vaccination schedule in 2005 for Indigenous children living in Qld, WA, SA and the NT [22]. The vaccine has been shown to be at least 89% effective among Indigenous people in the NT (compared with 72% effectiveness among non-Indigenous people) [16]. There has not been a notified case of HAV among Indigenous people in the NT since 2006 (there have been nine cases notified among non-Indigenous people, mostly contracted overseas). Previously, clinically significant HAV infections were much more common among Indigenous children than among non-Indigenous children, particularly those living in northern Qld, WA, SA and the NT [22]. Children aged 0-4 years were at greatest risk of HAV infection.

Hepatitis B

Transmission of hepatitis B virus (HBV) is from contact with blood and other body fluids (semen, vaginal fluids, and saliva) from an infected individual, commonly through sexual contact or use of contaminated injecting equipment [23]. A mother may also transmit HBV to the foetus during pregnancy or to the child during birth. Only 30-50% of people acutely infected with HBV will experience obvious symptoms, including jaundice, nausea, vomiting, and mild flu-like symptoms, but the virus can cause a more prolonged illness in which a person may look and feel well, but slowly develop chronic liver disease, cirrhosis, or liver cancer [17][23].

Of the 138 notifications of HBV for people living in WA, SA, and the NT between 2009 and 2011, six (4.3%) were among Indigenous people (excludes 1.4% of notifications in which Indigenous status was not reported) (Derived from [13][18][19][20][21]). The crude notification rate was the same for both the Indigenous and non-Indigenous populations at 1.1 per 100,000. Details of notifications by age-group are not available for these jurisdictions, but for the Indigenous population living in NSW, Vic, Qld, WA, SA, Tas and the NT, the rate of HBV diagnoses in 2011 was highest among those aged 30-39 years, with males having a substantially higher notification rate than females in this age-group [24].

Indigenous people residing in outer regional areas and major cities had the highest rates of HBV diagnoses in 2011, 5 and 4 per 100,000 respectively (based on cases notified in NSW, Vic, Qld, WA, SA, Tas, and the NT) [24]. For non-Indigenous people, the highest rate of notification, 2 per 100,000, was observed in remote areas.

A HBV vaccination program commencing in Indigenous communities in the mid-1980s has had considerable success in protecting Indigenous children from HBV infection [25], but several studies suggest that some Indigenous children had a sub-optimal response to the HBV vaccine, thus raising concerns about their immunity to HBV [26][27]. Possible explanations for the sub-optimal response of the vaccine include a failure in the cold-chain (maintaining the vaccine within a sufficiently cool temperature range), genetic factors, and extrinsic environmental factors, such as heavy smoking among pregnant women [26]. Despite the sub-optimal response/non-responsiveness of some Indigenous children to the HBV vaccine, it remains an effective means for reducing HBV infection levels [25].

Hepatitis C

Transmission of hepatitis C virus (HCV) typically occurs via blood-to-blood contact [28]. Injecting drug use is the most common method of contracting the virus and is responsible for the vast majority of cases [18][29]. The likelihood of transmission of HCV via sexual contact is generally very low [17]. Many people who are infected with HCV do not have symptoms and in many cases the virus is detected through blood tests for other medical matters [28]. Some people with HCV can live relatively normal lives, largely unaffected by the virus, but others may develop cirrhosis, liver cancer, or liver failure [30]. Treatment for HCV is available, but its success is dependent on several factors, including the HCV genotype. There is no vaccine to protect people against HCV [28].

Indigenous people accounted for approximately 13% of the 5,010 notifications of HCV among people living in WA, SA, and the NT in 2009-2011 (excluding 6.8% of notifications for which Indigenous status was not reported) (Derived from [13][18][19][20][21]). In these jurisdictions, the crude notification rate for HCV was significantly higher for Indigenous people than for non-Indigenous people (128 and 36 per 100,000 respectively). Over the three-year period from 2009-2011, notification rates were much lower for Indigenous people living in the NT than for those living in WA and SA.

The age pattern of newly diagnosed HCV was slightly different for the Indigenous and non-Indigenous populations in WA, SA, Tas, and the NT in 2011 [24]. Among Indigenous people, rates were highest for those in the 20-29, 30-39, and 40-49 years age-groups. For non-Indigenous people, the rates were highest in the 30-39, 40-49, and 50-59 years age-groups. Rates were generally higher for males than for females for both populations.

In contrast to some other reported communicable diseases, the rates of newly diagnosed HCV infection among Indigenous people were highest for those living in inner regional areas and major cities (for WA, SA, Tas, and the NT in 2011) [24]. These rates were 7.2 and 7.8 times the rates reported for non-Indigenous people in the same areas. For non-Indigenous people, the rate of HCV increased in accordance with remoteness.

Haemophilus influenzae type b

Haemophilus influenzae type b (Hib) is a bacterium that can cause meningitis, epiglottitis, pneumonia, septicaemia, cellulitis, osteomyelitis, pericarditis and septic arthritis [2][31][32]. Infants and children are particularly susceptible to Hib [2][31][33], which is spread by respiratory secretions. The main risk factors for Hib include contact with other children, particularly in large families or day care centres [34].

Extent of Hib disease among Indigenous people

Hib notifications in Australia declined steeply following the commencement of nationally funded infant vaccination in 1993; only 32 cases were reported in 2004-2005 compared with 617 in 1993-1994 [2][35]. The disease persists at low levels, but Indigenous children, particularly those aged under one year, continue to be at higher risk of contracting Hib than are non-Indigenous children [2][34][35][36].

In 2010, there were 24 notifications for Hib, with the crude notification rate 20 times higher for Indigenous people (1.4 per 100,000) than for non-Indigenous people [37]. The ratio has fluctuated on a year-by-year basis because of the small number of notifications, but has been consistently much higher than the pre-vaccination ratio of 2.7 in 1993-1994 [35][37].

Pneumococcal disease

Pneumococcal disease results from infection by the bacterium Streptococcus pneumoniae (also known as pneumococcus) which may cause pneumonia when in the respiratory tract [33]. Invasive pneumococcal disease (IPD) occurs when the bacterium infects other normally sterile sites, such as blood and cerebrospinal fluid, causing bacteraemia, septicaemia and meningitis [2][33]. Rates of IPD are highest in infants and the elderly. Recognised risk factors for pneumococcal disease include: diabetes; chronic respiratory; cardiac and renal diseases; other immune-compromised conditions; tobacco use; and high levels of alcohol consumption [2][38][39]. In children, recurrent or chronic OM and attendance at childcare increases susceptibility to IPD.

Nationally-funded vaccination for pneumococcal disease was made available to Indigenous adults aged 50 years and older and to Indigenous people aged 15-49 years at high risk in 1999 [33]. In 2001, vaccination was funded for Indigenous infants and young children and for all Australian children medically at risk. From 2005, nationally-funded vaccination was made available to all Australian infants and to all people aged 65 years and older, in addition to those populations eligible since 1999 [2][33][38].

Extent of invasive pneumococcal disease among Indigenous people

Detailed data are available for IPD, which has been notifiable Australia-wide since 2001 [38]. Indigenous children and adults have a significantly higher incidence of IPD than do non-Indigenous children and adults [40][38][41]. Based on notifications for people living in NSW, Vic, Qld, WA, SA, Tas and the NT in 2006-2008, the age-standardised rate of IPD for Indigenous people (46 per 100,000) was 7.3 times higher than the rate for other people [40]. Nationally, age-standardised notification rates for Indigenous people were 5.8 times higher in 2007 and 4.6 times higher in 2008 than those for their non-Indigenous counterparts [38].

Among Indigenous people living in NSW, Vic, Qld, WA, SA, Tas and the NT, notification rates for IPD in 2006-2008 were highest in the 65 years and older age-group (114 per 100,000), followed by the 45-54 years age-group (58 per 100,000) [40]. Importantly, rates for Indigenous people aged 35-44 and 45-54 years (50 and 58 per 100,000, respectively) were almost 12 times higher than those for other people.

There are no national pre-vaccination data available for Indigenous people because vaccination programs for pneumococcal began prior to national notification of IPD, but regional data and data after 2001 indicate that vaccination programs have had a significant impact on the number of cases of IPD among both the Indigenous and non-Indigenous populations [38][39][41][42][43]. Vaccination has reduced the burden of IPD in Australia, but the number of cases of non-vaccine type IPD has increased – this is most pronounced in non-Indigenous children [37][38][44] – and the recent increase in IPD in Indigenous adults has raised some concerns that the adult vaccination program may be less than adequate [38][39].

At the start of the national Indigenous childhood pneumococcal vaccination program in 2001, the rate of IPD for Indigenous children aged less than 2 years (219 per 100,000) was 2.9 times higher than the rate for non-Indigenous children [45]. By 2004, rates for Indigenous children under 2 years had decreased to 92 per 100,000, similar to rates for non-Indigenous children [45]; since that time, rates have remained relatively stable among Indigenous children but have decreased for non-Indigenous children, leading to an increasing gap [46]. The notification rate of IPD for Indigenous children aged 0-4 years was 3.7 times higher than that for other children in 2006-2008 [40]. In 2008, Indigenous children aged less than one year had 4.2 times the rate of IPD of non-Indigenous children, and Indigenous children aged one year had 3.0 times the rate of non-Indigenous children of the same age [38]. (It should be noted that there were small numbers of notifications of Indigenous children in the younger age-groups.)

IPD rates for Indigenous adults decreased after the introduction of vaccination programs in the Kimberley, WA [42] and in north Qld [43]. Rates for Indigenous and non-Indigenous people aged over four years in regional NSW were similar in 2007-2009 [41]. The higher rates of IPD notifications for Indigenous people are reflected in hospitalisation rates for pneumococcal septicaemia and meningitis [32].

National case fatality rates for IPD for Indigenous people were lower than those for non-Indigenous people in 2007-2008 (4.6% compared with 8.7% respectively) (Derived from [38]). Of the 224 reported deaths from IPD in 2007-2008, 15 were identified as Indigenous (deaths from IPD may be under-reported).

Meningococcal disease

Meningococcal disease is caused by the bacterium Neisseria meningitidis (also known as meningococcus) [33]. Manifestations of meningococcal disease include meningitis, meningococcaemia without meningitis, and septic arthritis. The risk of infection increases in crowded housing conditions [47]. In 2011, the most common groups of meningococcus found in Australia were B (84%) and C (4.2%), with proportions similar to those reported since 2007 [48][49]. Vaccination against serogroup C was funded for all infants from 2003; a catch-up program for all people aged up to 19 years ended in 2007 [48].

Extent of meningococcal disease among Indigenous people

The rate of meningococcal disease is higher for Indigenous people than for other Australians, and children aged less than 5 years are particularly susceptible [32]. The most recent information that includes Indigenous status is from 2003-2006. During that period, 106 (8.4%) of the 1,263 cases of meningococcal disease notified in NSW, Vic, WA, SA and the NT were identified as Indigenous [32]. Around one-third (32%) of all cases, and 69% of cases identified as Indigenous, occurred among children aged 0-4 years. The rate of 45 per 100,000 for Indigenous children aged 0-4 years was 4.9 times the rate for their non-Indigenous counterparts. The age-standardised rate of 5.1 per 100,000 for Indigenous people was 2.6 times the rate of other Australians.

Previously recorded outbreaks among Indigenous children in north-west Qld were due to serogroup C [50], but the disease in young children is now mainly due to serogroup B [48].

There were 21 deaths from meningococcal disease for people living in Qld, WA, SA and the NT in 2003-2005 [32]. One death was of a person identified as Indigenous.

Sexually transmitted infections

Sexually transmissible infections (STIs) are infections that are spread primarily by heterosexual or homosexual contact with an infected person [1]. STIs are caused by microorganisms that are transmitted from one person to another through semen, fluid from the vagina, anal or throat secretions, and blood [51]. Some STIs can also be transmitted under some circumstances via skin to skin contact, or from mother to baby during pregnancy and/or birth. Most STI cases are found among sexually active adolescents and young adults, and access to and use of condoms is regarded as fundamental in preventing STI transmission [52][53].

The majority of STIs are asymptomatic or produce only mild symptoms [54][55]. Many people affected find out they have an infection through screening and contact tracing. STIs can usually be effectively treated if diagnosed early, but, if left untreated, they may lead to complications [1].

Many factors have been identified as contributing to the development of STIs. Factors that are particularly relevant to the Indigenous population include: a younger more mobile population; socio-economic disadvantage; poor access to health services; and lack of clinical staff who have the competence and sensitivity to deal with sexual health issues among Indigenous people [56][57].

The NNDSS collects data on some STIs, including chlamydia, gonorrhoea, syphilis, donovanosis, and HIV/AIDS [58][59]. Human papilloma virus (HPV) and genital herpes are believed to be the most common STIs in Australia, but they are not notifiable diseases so it is difficult to monitor incidence [59]. Variations in notification rates over time may reflect real changes in incidence, but can also be due to the introduction of easier and more sensitive testing procedures, greater targeted screening, and public awareness campaigns [60]. The high level of screening in some Indigenous communities probably contributes to the higher STI rates reported for Indigenous people than for non-Indigenous people.

Gonorrhoea

Gonorrhoea is caused by the bacterium Neisseria gonorrhoeae [61]. In women, gonorrhoea can affect the urethra, cervix, and rectum, and in men it can affect the urethra and rectum. Gonorrhoea can also infect the throat in women and men. Gonorrhoea is highly contagious and, if left untreated, the infection can cause pelvic inflammatory disease in women and may cause damage to the testes in men. Untreated gonorrhoea can lead to infertility in both women and men.

For the period 2009-2011, Indigenous people accounted for 72% of gonorrhoea notifications in Qld, WA, SA, and the NT (excluding 14% of notifications for which Indigenous status was not stated) (Derived from [13][18][19][20][21]). The crude notification rate was substantially higher for Indigenous people in these jurisdictions than for their non-Indigenous counterparts, 1,093 and 17 per 100,000 respectively. The jurisdictions with the highest rates among Indigenous people were the NT (2,402 per 100,000) and WA (1,271 per 100,000).

In 2011, the majority of gonorrhoea notifications in the Indigenous population occurred in the 15-29 years age-group (78% of notifications in Vic, Qld, WA, SA, Tas, and the NT) [18]. In the non-Indigenous population, gonorrhoea was more common among slightly older people, with those aged 20-39 years accounting for 65% of gonorrhoea notifications. In the same year, Indigenous females were only marginally more likely to be diagnosed with gonorrhoea than were Indigenous males (1.2 times more likely); in the non-Indigenous population, the number of diagnoses for males was four times the number reported for females. This suggests the transmission of gonorrhoea occurs largely through heterosexual contact in the Indigenous population, whereas sex between males is an important mode of transmission among non-Indigenous people [24].

In 2007-2011, crude notification rates for gonorrhoea were highest for remote and very remote areas of residence for both Indigenous and non-Indigenous people [18]. The rate of diagnosis for Indigenous people in these areas was 61 and 33 times higher than the rate for non-Indigenous people.

Syphilis

Syphilis, caused by the organism Treponema pallidum, is a complex infection that has four identified stages: primary, secondary, latent, and tertiary [62]. In the initial stage of the infection, syphilis causes painless ulcers or sores around the mouth or genital area. If detected early, syphilis can be easily treated but, if left untreated, the infection can be very serious causing damage to the brain, heart, blood vessels, skin, intestinal tract, and bones [24]. For pregnant women, untreated syphilis poses further serious health threats as the infection can be passed on to the child, possibly resulting in physical deformities and brain damage [63].

In 2009-2011, 449 (13%) of the 3,479 people newly diagnosed with syphilis were identified as Indigenous (excludes notifications from the ACT and the 4.9% of notifications for which Indigenous status was not stated) (Derived from [13][18][19][20][21]). The crude notification rate for Indigenous people was 5.7 times the rate for non-Indigenous people (27 and 4.7 per 100,000 respectively). In the Indigenous population, the jurisdictions with the highest notification rates were the NT (51 per 100,000) and Qld (43 per 100,000).

Syphilis is more common among adolescents and young adults in the Indigenous population, with those aged 15-29 years accounting for 65% of syphilis diagnoses in all health jurisdictions in 2011 [18]. Among non-Indigenous people, over 80% of syphilis cases occurred in people aged 20-49 years. This pattern of diagnosis has remained relatively consistent from 2007-2011 for both populations, but the number of diagnoses among Indigenous people aged 15-19 years in 2011 was more than 3.5 times the number reported in 2009 (67 and 18 respectively).

In 2011, the number of syphilis diagnoses in the Indigenous population was similar for both males and females (95 and 101 respectively) [18]. A different pattern was observed in the non-Indigenous population with males accounting for 93% of diagnoses (male to female ratio 16:1). This suggests differences in modes of transmission for syphilis in the Indigenous and non-Indigenous populations [24].

The rates of syphilis notifications were highest among Indigenous people living in remote and very remote areas in 2007-2011 [18]. In 2011, notification rates for Indigenous people living in remote and very remote areas were 119 and 19 times the rates for their non-Indigenous counterparts. Notification rates for non-Indigenous people were highest in major cities and in very remote areas.

Chlamydia

Chlamydia is caused by the bacterium Chlamydia trachomatis [54]. In women it can cause cervicitis, endometritis, and pelvic inflammatory disease, which can lead to tubal factor infertility and ectopic pregnancy. In men, it can cause urethritis, epididymo-orchitis, and prostatitis. Due to the lack of obvious symptoms for many cases of the disease, the incidence of chlamydia is underestimated in notification data. Chlamydia is the most common STI among Indigenous people in Australia [56], but when considering only the jurisdictions with reasonable Indigenous identification25 it is second to gonorrhoea [18].

Indigenous people accounted for 20% of the notifications of chlamydia during 2009-2011 (based on 49,380 cases notified in WA, SA, Tas, and the NT, and excluding 13% of notifications for which Indigenous status was not stated) (Derived from [13][18][19][20][21]). The crude notification rate for chlamydia was considerably higher for Indigenous people than for non-Indigenous people in 2009-2011: 1,643 per 100,000 compared with 296 per 100,000. The highest rate of chlamydia notifications was for Indigenous people living in the NT (2,089 per 100,000).

Chlamydia is typically diagnosed among adolescents and young adults in both the Indigenous and non-Indigenous populations [18]. In 2011, persons aged 15-29 years accounted for 82% of chlamydia notifications in both populations (notifications in Vic, WA, SA, Tas, and the NT). There were notable increases between 2007 and 2011 in the number of chlamydia notifications among Indigenous people aged 15-19 and 20-29 years, with increases of 29% and 41% respectively.

For both the Indigenous and non-Indigenous populations, females accounted for a greater proportion of chlamydia diagnoses than did males in 2011 (62% and 58% of the diagnoses respectively) [18]. The female to male ratio was 1.7:1 for Indigenous people, and 1.4:1 for non-Indigenous people.

As is the case for other STIs, Indigenous people living in remote and very remote areas had the highest rates of chlamydia diagnoses in 2011 (3,345 and 3,053 per 100,000, respectively) [18]. For the Indigenous population, inner regional, outer regional, and major cities reported the largest increases in chlamydia notification rates over the five-year period 2007-2011, with the greatest increase observed in inner regional areas (182%). For non-Indigenous people, notification rates were highest in very remote areas and in major cities in 2011.

HIV/AIDS

The human immunodeficiency virus (HIV) is a retrovirus that destroys cells in the body’s immune system [64]. Untreated, the virus weakens immune system functioning to the point where minor infections may become fatal [65]. This late stage of HIV is referred to as acquired immune deficiency syndrome (AIDS). At present there is no vaccine to prevent HIV, nor is there a cure, but anti-retroviral therapy has dramatically reduced the number of HIV cases progressing to AIDS [28][64].

The transmission of HIV occurs in one of three ways: unprotected sexual contact with an infected person; infected blood passing into another person’s bloodstream; and an infected mother can pass HIV on to her child either during birth or through breast-feeding [66]. Unprotected anal sex presents the greatest risk of exposure to HIV. Other behaviours that can put people at high risk of HIV include: unprotected vaginal sex; unprotected oral sex; and sharing injecting equipment (such as syringes and needles).

To date, Australia has successfully prevented an uncontrolled spread of HIV, and the overall rates of HIV are low in comparison with other countries [58][24]. However, great concerns have been expressed about the possible impact of HIV/AIDS among Indigenous people, for whom AIDS has been seen as having the potential ‘to further erode the social and economic fabric of Indigenous communities’ ([64], p.6). Indigenous people are regarded as being at particular risk of HIV infection due to their higher rates of STIs, limited access to health care, and over-representation in prisons and juvenile detention [67].

Extent of HIV/AIDS among Indigenous people

National surveillance data show that in 2011 there were 1,137 cases of newly diagnosed HIV infection of which 22 (1.9%) were among Indigenous people [18]. Age-standardised rates of HIV diagnosis were similar for Indigenous and non-Indigenous people at 4.4 and 5.0 per 100,000 respectively [24]. There has been a marginal increase in the rate of HIV diagnosis among Indigenous people from 3.9 per 100,000 in 2007 to 4.4 per 100,000 in 2011. In this period, a nominal increase was also observed in the diagnosis rate among non-Indigenous people.

In 2011, males accounted for 77% of new HIV cases among Indigenous people [18]. The median age of diagnosis for Indigenous males was 33 years. In comparison, non-Indigenous males accounted for a larger proportion of new HIV cases among non-Indigenous people (88%), and the median age of diagnosis among non-Indigenous males was 37 years (Derived from [18]). The diagnosis rate of HIV has remained relatively consistent over the five years from 2007 to 2011 for both Indigenous and non-Indigenous males, with a lower rate of diagnosis observed among Indigenous males (5.9 per 100,000 in 2007, 6.3 per 100,000 in 2011) than among non-Indigenous males (7.7 per 100,000 in 2007, 8.0 in 2011) [24].

More than 80% of new HIV infections among the Indigenous population in 2011 were reported in Qld (36%), NSW (23%), and WA (23%) [18]. Indigenous people living in major cities and in very remote areas had the highest rates of new HIV diagnoses, 8 and 6 per 100,000 respectively. In terms of exposure to HIV, men who have sex with men accounted for two-thirds (67%) of new HIV cases among Indigenous people in 2011 [18]. Heterosexual contact was also identified as a common form of exposure to HIV among Indigenous people (24%). The percentage of new HIV cases attributed to injecting drug use decreased substantially from 2010 to 2011, with just 4.8% of new HIV cases coming from injecting drug use in 2011 compared with 20% in 2010.

The patterns of new HIV infections are slightly different for Indigenous and non-Indigenous people (Derived from [18]). Most new cases of HIV infections among non-Indigenous people in 2011 were reported in NSW (34%), Vic (29%) and Qld (19%). Among the non-Indigenous population, those residing in major cities had the highest rate of HIV infection (7 per 100,000) [18]. The rates of diagnosis were much lower for the remaining areas of residence, ranging from 1 to 3 per 100,000.

Among non-Indigenous people, 94% of all new HIV cases in 2011 were attributed to the categories ‘men who have sex with men’ (71%) and ‘heterosexual contact’ (23%) (Derived from [18]). Injecting drug use was responsible for 1.8% of new cases among non-Indigenous people.

Overall in Australia, the cumulative number of HIV diagnoses by the end of 2011 was 31,645, of which 219 were among Indigenous people [18].

Information about the occurrence of AIDS in the Indigenous population in 2011 is not available, but the number of new AIDS cases for the total population in 2009 was only 90 [20]. In 2009, there were nine deaths following AIDS in Australia. The number of new AIDS cases in the Indigenous population in the ten-year period 1997-2006 was low, but Indigenous people had a slightly higher rate of AIDS diagnoses than did non-Indigenous people in 2006 (1.2 compared with 1.0 per 100,000) [68]. The absence of reporting by Indigenous status in the most recent AIDS data [20] may be due to the marked decrease in new AIDS diagnoses and deaths in Australia over the past decade.

Skin infections and infestations

Susceptibility to skin infections and infestations increases with poor living conditions and overcrowding [69][70]. Skin infections in many Indigenous communities reflect serious health inequalities, [71] but biomedical research has been limited in recent years [72].

Scabies – a disease caused by the mite Sarcoptes scabiei, resulting in inflammation and itching [73] – is endemic in some remote central and northern Indigenous communities, with prevalence up to 50% in children [74] and up to 25% in adults [75]. The East Arnhem Regional Healthy Skin Program reported that more than 70% of children presented in 2002-2005 with scabies, almost all before they reached 2 years of age [76]. Another study of children in a remote community in the NT in 2007 found that 68% of children had presented with scabies during their first year of life, and 77% had presented in the first two years [77].

Scratching in response to the inflammation and itching of scabies infestation can result in pyoderma (also referred to as impetigo or skin sores), a bacterial infection of the skin that can lead to kidney disease and possibly heart disease [78]. A study of a remote community in the NT in 2007 found that 82% of children presented with pyoderma in their first year of life and 87% in their first two years [77]. The pyoderma in Indigenous communities commonly involves group A streptococcus (GAS), which is responsible for continuing outbreaks of acute post-streptococcal glomerulonephritis and ARF [78][79].

Indigenous people, particularly those living in the high-rainfall, humid areas of northern Australia, are also vulnerable to a variety of fungal and related organisms [78].

Skin conditions can be linked with serious complications, which can result in hospitalisation and, very uncommonly, death. ICD ‘Diseases of the skin and subcutaneous tissue’ was responsible for 7,730 hospital separations among Indigenous people living in NSW, Vic, Qld, WA, SA and the NT in 2010-11, accounting for 4.2% of all Indigenous hospitalisations (excluding those from dialysis) [80]. After age-adjustment, the Indigenous separation rate of 16 per 1,000 was 2.5 times higher than that of other Australians. In 2006-2010, 10% of medical admissions to Mt Isa Hospital for children aged under 5 years were due to scabies or pyoderma, and all were Indigenous [81]. At Alice Springs Hospital in 2003-2006, Staphylococcus aureus bacteraemia (SAB) was recorded at a mean annual incidence rate of 161 per 100,000 for Indigenous and 8 per 100,000 for non-Indigenous inpatients; SAB was community-acquired in over 70% of both patient groups, and pyoderma or scabies was identified in 32% and 4% respectively of Indigenous patients [82].

References

1. Burns J, Burrow S, Genovese E, Pumphrey M, Sims E, Thomson N (2003) Other communicable diseases. In: Thomson N, ed. The health of Indigenous Australians. South Melbourne: Oxford University Press: 397-441
2. The Australian immunisation handbook (2008) National Health and Medical Research Council
3. Central Australian Rural Practitioners Association (2010) CARPA standard treatment manual [5th ed.]. 5th ed. Alice Springs: Central Australian Rural Practitioners Association
4. Australian Institute of Health and Welfare (2012) Australia's health 2012. Canberra: Australian Institute of Health and Welfare
5. National Institute of Allergy and Infectious Diseases (2009) Tuberculosis (TB): detailed explanation of TB. Retrieved 6 March 2009 from http://www.niaid.nih.gov/topics/tuberculosis/Understanding/WhatIsTB/Pages/detailed.aspx
6. Baker M, Das D, Venugopal K, Howden-Chapman P (2008) Tuberculosis associated with household crowding in a developed country. Journal of Epidemiology and Community Health; 62(8): 715-721
7. Krause V (2008) Tuberculosis (TB). In: Couzos S, Murray R, eds. Aboriginal primary health care: an evidence-based approach. 3rd ed. South Melbourne: Oxford University Press: 674-707
8. World Health Organization (2009) Global tuberculosis control - epidemiology, strategy, financing: WHO report 2009. Geneva: World Health Organization
9. Roche P, Bastian I, Krause V (2007) Tuberculosis notifications in Australia, 2005. Communicable Diseases Intelligence; 31(1): 71-80
10. Roche PW, Krause V, Konstantinos A, Bastian I, Antic R, Brown L, Christensen A, Gebbie S, Hurwitz M, Misrachi A, Waring J (2008) Tuberculosis notifications in Australia, 2006. Communicable Diseases Intelligence; 32(1): 1-11
11. Barry C, Konstantinos A, National Tuberculosis Advisory Committee (2009) Tuberculosis notifications in Australia, 2007. Communicable Diseases Intelligence; 33(3): 1-12
12. Barry C, Waring J, Stapledon R, Konstantinos A (2012) Tuberculosis notifications in Australia, 2008 and 2009. Communicable Diseases Intelligence; 36(1): 82-94
13. Australian Bureau of Statistics (2009) Experimental estimates and projections, Aboriginal and Torres Strait Islander Australians: Projected population, Aboriginal and Torres Strait Islander Australians, Australia, states and territories, 2006-2021 series [data cube]. Retrieved 8 September 2009 from http://www.abs.gov.au/ausstats/subscriber.nsf/log?openagent&32380ds002_2006.srd&3238.0&Data%20Cubes&E79A5308D989173FCA25762A001CE1C3&0&1991%20to%202021&08.09.2009&Latest
14. Australian Bureau of Statistics (2007) Australian demographic statistics, June quarter 2007. Canberra: Australian Bureau of Statistics
15. Hepatitis Australia (2010) About hepatitis. Retrieved 18 November 2011 from http://www.hepatitisaustralia.com/about-hepatitis
16. Markey P (2010) Nearing elimination of hepatitis A in the Northern Territory following immunisation of Indigenous infants. Northern Territory Disease Control Bulletin; 17(3): 1-6
17. Australasian contact tracing manual : a practical handbook for health care providers managing people with HIV, viral hepatitis, STIs and HIV-related tuberculosis (2010) Australasian Society for HIV Medicine
18. The Kirby Institute (2012) HIV, viral hepatitis and sexually transmissible infections in Australia: annual surveillance report 2012. Sydney: University of New South Wales
19. The Kirby Institute (2011) HIV, viral hepatitis and sexually transmissible infections in Australia: annual surveillance report 2011. Sydney: University of New South Wales
20. National Centre in HIV Epidemiology & Clinical Research (2010) HIV, viral hepatitis and sexually transmissible infections in Australia: annual surveillance report 2010. Sydney, NSW: National Centre in HIV Epidemiology & Clinical Research, University of New South Wales
21. Australian Bureau of Statistics (2011) Australian demographic statistics, March quarter 2011. Canberra: Australian Bureau of Statistics
22. MacIntyre CR, Burgess M, Isaacs D, MacIntyre PB, Menzies R, Hull B (2007) Epidemiology of severe hepatitis A in Indigenous Australian children. Journal of Paediatrics and Child Health; 43(5): 383-387
23. Department of Health and Ageing (2008) The Australian Immunisation Handbook 9th edition 2008: 3.6 Hepatitis B. In: The Australian Immunisation Handbook 9th edition 2008. Canberra: Immunise Australia Program, Department of Health and Ageing, Australia: 15
24. The Kirby Institute (2012) Bloodborne viral and sexually transmitted infections in Aboriginal and Torres Strait Islander people: surveillance and evaluation report 2012. Sydney: University of New South Wales
25. Sullivan JS, Hanna JN (1999) A genetic marker associated with non-response to recombinant hepatitis B vaccine by indigenous Australian children [letter]. Journal of Paediatrics and Child Health; 35(4): 412-3
26. Hanna J, Faoagali J, Buda P, Sheridan J (1997) Further observations on the immune response to recombinant hepatitis B vaccine after administration to Aboriginal and Torres Strait Island children. Journal of Paediatrics and Child Health; 33(1): 67-70
27. Dent E, Selvey CE, Bell A, Davis J, McDonald MI (2010) Incomplete protection against hepatitis B among remote Aboriginal adolescents despite full vaccination in infancy. Communicable Diseases Intelligence; 34(4): 435-439
28. Communicable Diseases Section Department of Human Services (2005) The blue book - guidelines for the control of infectious diseases. Melbourne: Victorian Government Department of Human Services
29. Hepatitis C Virus Projections Working Group (2006) Estimates and projections of the hepatitis C virus epidemic in Australia 2006. Canberra: Ministerial Advisory Committee on AIDS, Sexual Health and Hepatitis C Sub-Committee
30. Wilson H, Hopwood M, Hull P, Lavis Y, Newland J, Bryant J, Treloar C (2010) Treatment decisions: what makes people decide to have treatment for hepatitis C?. Brisbane: Hepatitis Council of Queensland
31. Horby P, Gilmour R, Wang H, McIntyre P (2003) Progress towards eliminating Hib in Australia: an evaluation of Haemophilus influenzae type b prevention in Australia, 1 July 1993 to 30 June 2000. Communicable Diseases Intelligence; 27(3): 324-341
32. Menzies R, Turnour C, Chiu C, McIntyre P (2008) Vaccine preventable diseases and vaccination coverage in Aboriginal and Torres Strait Islander people, Australia, 2003 to 2006. Canberra: Department of Health and Ageing
33. Chiu C, Dey A, Wang H, Menzies R, Deeks S, Mahajan D, Macartney K, Brotherton J, Jardine A, Quinn H, Jelfs J, Booy R, Lawrence G, Jayasinghe S, Roberts A, Senanayake S, Wood N, McIntyre P (2010) Vaccine preventable diseases in Australia, 2005 to 2007. Canberra: Australian Department of Health and Ageing
34. Jacups SP, Morris PS, Leach AJ (2011) Haemophilus influenzae type b carriage in Indigenous children and children attending childcare centers in the Northern Territory, Australia, spanning pre- and post-vaccine eras. Vaccine; 29(16): 3083-3088
35. Wang H, Deeks S, Glasswell A, McIntyre P (2008) Trends in invasive Haemophilus influenzae type b disease in Australia, 1995-2005. Communicable Diseases Intelligence; 32(3): 316-325
36. Brotherton J, McIntyre P, Puech M, Wang H, Gidding H, Hull BP, Lawrence G, MacIntyre R, Wood N, Armstrong D (2004) Vaccine preventable diseases and vaccination coverage in Australia, 2001 to 2002. Canberra: National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Australian Institute of Health and Welfare, Department of Health and Ageing
37. NNDSS Annual Report Writing Group (2012) Australia's notifiable diseases status, 2010: annual report of the National Notifiable Diseases Surveillance System. Communicable Diseases Intelligence; 36(1): 1-69
38. Barry C, Krause VL, Cook HM, Menzies RI (2012) Invasive pneumococcal disease in Australia 2007 and 2008. Communicable Diseases Intelligence; 36(2): E151-E165
39. Jacups SP, Cheng A (2011) The epidemiology of community acquired bacteremic pneumonia, due to streptococcus pneumoniae, in the top end of the Northern Territory, Australia - over 22 years. Vaccine; 29(33): 5386-5392
40. Australian Institute of Health and Welfare (2011) Aboriginal and Torres Strait Islander health performance framework 2010: detailed analyses. Canberra: Australian Institute of Health and Welfare
41. Massey PD, Kerry T, Osbourn M, Taylor K, Durrheim DN (2011) Invasive pneumococcal disease in New South Wales, Australia: reporting Aboriginal and Torres Strait Islander status improves epidemiology: surveillance report. Western Pacific Surveillance and Response; 2(3): 1-4
42. Mak DB (2004) Invasive pneumococcal disease in the Kimberley, 1995-2001. Australian Journal of Rural Health; 12(6): 237-240
43. Hanna JN, Humphreys JL, Murphy DM (2006) Invasive pneumococcal disease in Indigenous people in north Queensland, 1999-2004. Medical Journal of Australia; 184(3): 118-121
44. Fitzgerald T, Masseya PD, Islama F (2012) Changes in invasive pneumococcal disease serotypes in a regional area of Australia following three years of 7vPCV introduction. Western Pacific Surveillance and Response Journal; 3(2): 1-6
45. Roche PW, Krause VL, Bartlett M, Coleman D, Cook H, Davis C, Fielding JE, Holland R, Giele C, Gilmour R, Kampen R, Brown M, Gilbert L, Hogg G, Murphy D (2006) Invasive pneumococcal disease in Australia, 2004. Communicable Diseases Intelligence; 30(1): 80-92
46. Roche P, Krause V, Cook H (2007) Invasive pneumococcal disease in Australia, 2005. Communicable Diseases Intelligence; 31(1): 86-100
47. Standing Committee on Aboriginal and Torres Strait Islander Health, Statistical Information Management Committee (2006) National summary of the 2003 and 2004 jurisdictional reports against the Aboriginal and Torres Strait Islander health performance indicators. Canberra: Australian Institute of Health and Welfare
48. Lahra MM, Enriquez RP (2012) Annual report of the Australian Meningococcal Surveillance Programme, 2011. Communicable Diseases Intelligence; 36(3): E251–E262
49. Australian Meningococcal Surveillance Programme (2010) Annual report of the Australian Meningococcal Surveillance Programme, 2009. Communicable Diseases Intelligence; 34(3): 291-302
50. Pearce M, Sheridan J, Jones D, Lawrence G, Murphy D, Masutti B, McCosker C, Douglas V, O'Keefe A, Young F, Thomson M, Gorman B, Hansman D, Hill P (1995) Control of group C meningococcal disease in Australian Aboriginal children by mass rifampicin chemoprophylaxis and vaccination. Lancet; 346(8966): 20-23
51. Family Planning Association of WA (2010) Sexually transmissible infections (STI) and blood-borne viruses (BBV): a guide for health professionals, educators, and general practitioners. Northbridge, WA: Family Planning Association of WA
52. de Wit J, Holt M, Treloar C(Eds) (2012) HIV/AIDS, hepatitis and sexually transmissible infections in Australia: annual report of trends in behaviour 2012. Sydney: National Centre in HIV Social Research, The University of New South Wales
53. Australasian Society for HIV Medicine (2009) Toward a second national sexually transmissible infections strategy 2009 - 2013. Sydney: Australasian Society for HIV Medicine
54. Bowden FJ, Tabrizi SN, Garland SM, Fairley CK (2002) Sexually transmitted infections: new diagnostic approaches and treatments. Medical Journal of Australia; 176(11): 551-557
55. Australian Department of Health and Ageing (2010) Second national sexually transmissible infections strategy 2010 - 2013. Canberra: Department of Health and Ageing, Australia
56. Australian Health Ministers’ Advisory Council (2011) Aboriginal and Torres Strait Islander health performance framework: 2010 report. Canberra: Office for Aboriginal and Torres Strait Islander Health, Department of Health and Ageing
57. National Centre in HIV Epidemiology & Clinical Research (2010) Bloodborne viral and sexually transmitted infections in Aboriginal and Torres Strait Islander people: surveillance and evaluation report 2010. Sydney, NSW: National Centre in HIV Epidemiology & Clinical Research, University of New South Wales
58. Australian Institute of Health and Welfare (2010) Australia's health 2010: the twelfth biennial report of the Australian Institute of Health and Welfare. Canberra: Australian Institute of Health and Welfare
59. Australian Institute of Health and Welfare (2006) Australia's health 2006: the tenth biennial health report of the Australian Institute of Health and Welfare. Canberra: Australian Institute of Health and Welfare
60. NNDSS Writing Group (2011) Australia's notifiable diseases status, 2009: annual report of the National Notifiable Diseases Surveillance System. Communicable Diseases Intelligence; 35(2): 61-131
61. Gonorrhoea (2006) Family Planning Association of WA
62. Syphilis [fact sheet] (2009) Western Australia Communicable Disease Control Public Health
63. Merianos A, Bowden F, Krause V, Savage J, Wallace T (2001) Communicable diseases. In: Condon JR, Warman G, Arnold L, eds. The health and welfare of Territorians. Darwin: Territory Health Services: 71-86
64. Australian National Council on AIDS Hepatitis C and Related Diseases (2000) The management of HIV/AIDS: a resource guide for Indigenous primary health care organisations. Canberra: ANCAHRD, Commonwealth Department of Health and Aged Care
65. Western Australian Department of Health (2008) HIV model of care. Perth, WA: Health Networks, Western Australian Department of Health
66. HIV & AIDS (2012) Western Australia Communicable Disease Control
67. Australian Department of Health and Ageing (2010) Sixth national HIV strategy 2010-2013. Canberra: Department of Health and Ageing, Australia
68. National Centre in HIV Epidemiology and Clinical Research (2007) HIV/AIDS, viral hepatitis and sexually transmissible infections in Australia: Annual Surveillance Report 2007. Sydney: Australian Institute of Health and Welfare
69. McDonald E, Bailie R, Brewster D, Morris P (2008) Are hygiene and public health interventions likely to improve outcomes for Australian Aboriginal children living in remote communities? A systematic review of the literature. BMC Public Health; 8: 153 Retrieved 8 May 2008 from http://www.biomedcentral.com/1471-2458/8/153
70. Currie B, Couzos S (2008) Skin infections. In: Couzos S, Murray R, eds. Aboriginal primary health care: an evidence-based approach. 3rd ed. South Melbourne: Oxford University Press: 410-444
71. Australian Institute of Health and Welfare (2011) Australian hospital statistics 2009-10. Canberra: Australian Institute of Health and Welfare
72. Mounsey K, Ho MF, Kelly A, Willis C, Pasay C, Kemp DJ, McCarthy JS, Fischer K (2010) A tractable experimental model for study of human and animal scabies. PLoS Neglected Tropical Diseases; 4(7): e756 (1-6)
73. Walton SF, DBeroukas D, Roberts-Thomson P, Currie BJ (2008) New insights into disease pathogenesis in crusted (Norwegian) scabies: the skin immune response in crusted scabies. British Journal of Dermatology; 158(6): 1247-1255
74. Hengge UR, Currie BJ, Jäger G, Lupi O, Schwartz RA (2006) Scabies: a ubiquitous neglected skin disease. The Lancet Infectious Diseases; 6(12): 769-779
75. Carapetis JR, Connors C, Yarmirr D, Krause V, Currie BJ (1997) Success of a scabies control program in an Australian Aboriginal community. Pediatric Infectious Disease Journal; 16(5): 494-499
76. Clucas DB, Carville KS, Connors C, Currie B, Carapetis J, Andrews R (2008) Disease burden and health-care clinic attendances for young children in remote Aboriginal communities of northern Australia. Bulletin of the World Health Organization; 86(4): 275-281
77. McMeniman E, Holden L, Kearns T, Clucas DB, Carapetis JR, Currie BJ, Connors C, Andrews RM (2011) Skin disease in the first two years of life in Aboriginal children in East Arnhem Land. Australasian Journal of Dermatology; 52(4): 270–273
78. Currie BJ, Carapetis JR (2000) Skin infections and infestations in Aboriginal communities in northern Australia. Australasian Journal of Dermatology; 41(3): 139-145
79. McDonald M, Currie BJ, Carapetis JR (2004) Acute rheumatic fever: a chink in the chain that links the heart to the throat?. Lancet Infectious Diseases; 4(4): 240-245
80. Australian Institute of Health and Welfare (2012) Australian hospital statistics 2010-11 supplementary tables. Canberra: Australian Institute of Health and Welfare
81. Whitehall J, Kuzulugil D, Sheldrick K, Wood A (2013) Burden of paediatric pyoderma and scabies in North West Queensland. Journal of Paediatrics and Child Health; 49(2): 141–143
82. Hewagama S, Einsiedel L, Spelman T (2012) Staphylococcus aureus bacteraemia at Alice Springs Hospital, Central Australia, 2003-2006. Internal Medicine Journal; 42(5): 505–512

Endnote

24. Reflecting the fact that the vast majority of new cases of TB in Australia are among people born overseas, particularly relatively recent arrivals from India, Vietnam, the Philippines and China, the analysis here compares the notification rates of Indigenous people with those of Australian-born non-Indigenous people.

25. Jurisdictions where Indigenous status is reported for more than 50% of diagnoses.