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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, meningococcal disease and skin infections . Communicable diseases can be caused by bacteria (e.g. pertussis (whooping cough) and tuberculosis), viruses (e.g. influenza and HIV), fungi (e.g. tinea), protozoan parasites (e.g. malaria) and larger parasites (e.g. head lice) . Risk factors for communicable diseases vary according to the type of disease . Improvements to sanitation, and the increased use of vaccination and antibiotics (for bacterial infections), have markedly reduced some infectious diseases in Australia .
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 (TB) is primarily a lung infection caused by the inhalation of the bacterium Mycobacterium tuberculosis . 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 , all common in many Indigenous communities. Other risk factors also common among Indigenous people are diabetes, tobacco use, alcohol use and advanced kidney disease . Another risk factor for TB is HIV infection .
The most recent information about TB among Indigenous people is for 2005-2009, for which period 152 (19%) of the 800 notifications of TB among Australian-born people in Australia were identified as Indigenous (Derived from ).27 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 33). 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 ). After age-adjustment, the notification rate for Indigenous people was 11.1 times that for Australian-born non-Indigenous people (Table 34) (Derived from ).28
The notification rate of TB was higher for Indigenous people than that 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 34) (Derived from ).
|Source: Derived from Roche, 2007 , Roche, 2008 , Barry, 2009 , Barry, 2012 , ABS, 2009 , ABS, 2007 |
|Age-group (years)||Indigenous||Non-Indigenous||Rate ratio|
|Source: Derived from Roche, 2007 , Roche, 2008 , Barry, 2009 , Barry, 2012 , ABS, 2009 , ABS, 2007 |
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 . 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.
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) . 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.
The impact of HAV among Indigenous people has declined markedly since 2000, particularly after the introduction in 2005 of HAV vaccination into the national childhood vaccination schedule for Indigenous children living in Qld, WA, SA and the NT . 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 . Children aged 0-4 years were at greatest risk of HAV infection. 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) .
The great decline among Indigenous people is reflected in notification figures for the three-year period 2009-2011. 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 ). 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.
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 . 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 .
Of the 609 people diagnosed with newly acquired HBV in Australia in the three-year period 2010-2012, 53 (8.7%) were identified as Indigenous (Derived from ).29 The crude rate of newly diagnosed HBV of 2.7 per 100,000 for Indigenous people was 3.1 times the rate of 0.9 per 100,000 for non-Indigenous people. Details of the ages of the people with newly diagnosed HBV are not available for 2010-2012, but the majority of diagnoses in 2012 for both Indigenous and non-Indigenous people were among those aged 20 years or older (84% and 97%, respectively) . The male to female ratio of diagnoses of newly acquired HBV is generally around 3 in the non-Indigenous population, but the ratio for Indigenous people was 0.4 in 2012 .
The highest rate of diagnosis on newly acquired HBV for Indigenous people in 2012 was for those living in very remote areas; the next highest rates were for people living in outer regional areas and major cities . For non-Indigenous people, the rates are very similar across all areas of residence, with rates for remote areas being marginally higher than the rates for other areas.
A HBV vaccination program commencing in Indigenous communities in the mid-1980s has had considerable success in protecting Indigenous children from HBV infection , 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 . 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 tobacco use among pregnant women . 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 .
Transmission of hepatitis C virus (HCV) typically occurs via blood-to-blood contact . Injecting drug use is the most common method of contracting the virus and is responsible for the vast majority of cases . The likelihood of transmission of HCV via sexual contact is generally very low . 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 . Some people with HCV can live relatively normal lives, largely unaffected by the virus, but others may develop cirrhosis, liver cancer, or liver failure . 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 .
Unlike the case for HBV, the identification of Indigenous status in notifications of HCV is not good: the proportions of notifications in 2012 for which Indigenous status was not reported was more than 20% for all jurisdictions except WA (3%), SA (6%) and the NT (4%) .
Of the 5,316 people diagnosed with HCV in WA, SA and the NT in the three-year period 2010-2012, 729 (14%) were identified as Indigenous (Derived from ). In these jurisdictions, the crude notification rate for HCV was significantly higher for Indigenous people than that for non-Indigenous people (137 and 36 per 100,000, respectively). Over the three-year period 2010-2012, the notification rate was much lower for Indigenous people living in the NT (44 per 100,000) than that for Indigenous people living in WA (177 per 100,000) and SA (151 per 100,000).
In line with these overall notification rates, age-specific rates were much higher for Indigenous people living in WA, SA, Tas, and the NT in 2012 than those for their non-Indigenous counterparts, particularly in the ten-year age-groups between 20 and 49 years . The median age of notifications was around 10 years lower for Indigenous people than that for non-Indigenous people. Notification 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 for Indigenous people were highest for those living in inner regional areas and major cities (for WA, SA, Tas, and the NT in 2011) . These rates were between 7 and 10 times the rates reported for non-Indigenous people in the same areas. For non-Indigenous people, the rate of HCV increased by remoteness of residence.
Haemophilus influenzae type b (Hib) is a bacterium that can cause meningitis, epiglottitis, pneumonia, bacteraemia, cellulitis, osteomyelitis, pericarditis, and septic arthritis . Infants and children are particularly susceptible to Hib, which is serious in its invasive form . High rates of Hib carriage in the upper respiratory tract have been noted prior to cases of invasive disease . Higher rates in Indigenous populations worldwide suggest socioeconomic disadvantage, particularly high rates of tobacco use and crowded living conditions, as the probable cause .
Notifications of invasive Hib disease in Australia decreased by more than 95% following the commencement of nationally funded infant vaccination in 1993 . The decline has been markedly evident in Indigenous children, but they continue to be at higher risk of contracting Hib than are non-Indigenous children .
In 2007-2010, 25 (29%) of the 85 cases of invasive Hib disease notified in all jurisdictions were identified as Indigenous . Children (Indigenous and other) aged 0-4 years accounted for 40% of all cases; Indigenous children aged 0-4 years accounted for 18% of all cases and 60% of cases identified as Indigenous. The age-specific rate of 5.6 per 100,000 for Indigenous children aged 0-4 years was 15.7 times that for other children, with rates higher for Indigenous people in every age-group. After age-adjustment, the overall notification rate was 12.9 times higher for Indigenous people than that for other Australians.
There were no deaths coded as Haemophilus meningitis (likely to be due to Hib) for people living in NSW, NT, Qld, SA and WA in 2006-2010 .
Pneumococcal disease results from infection by the bacterium Streptococcus pneumoniae (also known as pneumococcus), which may cause pneumonia when in the respiratory tract . Invasive pneumococcal disease (IPD) occurs when the bacterium infects other normally sterile sites, such as blood and cerebrospinal fluid, causing bacteraemia and meningitis. Rates of IPD are highest in infants and older people. 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 . In children, recurrent or chronic OM and attendance at childcare increases susceptibility to IPD .
Nationally-funded vaccination for pneumococcal disease was made available in 1999 to Indigenous adults aged 50 years and older and to Indigenous people aged 15-49 years at high risk . 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 eligible since 1999.
Detailed data are available for IPD because it has been notifiable Australia-wide since 2001 . Indigenous people have a significantly higher incidence of IPD than do non-Indigenous people . Based on notifications for all jurisdictions in 2007-2010, the age-adjusted rate of IPD was 3.6 times higher for Indigenous people than that for other people. Among Indigenous people, age-specific rates for IPD were highest in the 50 years and older age-group (53 per 100,000), followed by the 0-4 years age-group (51 per 100,000). Importantly, age-specific rates for Indigenous people aged 25-49 (45 per 100,000) were almost 12 times higher than those for their non-Indigenous counterparts. To some degree, the high rate ratio in this age-group corresponds to the difference in the prevalence of adult risk factors between Indigenous and non-Indigenous people.
After age-adjustment, the IPD hospitalisation rate for Indigenous people living in NSW, NT, Qld, SA, Vic and WA between 2005 and 2010 was 6.0 times higher than the rate for their non-Indigenous counterparts . Among Indigenous people, age-specific rates of hospitalisations for IPD were highest in the 0-4 years age-group (27 per 100,000), followed by the 25-49 years (25 per 100,000) and the 50 years and older age-groups (24 per 100,000). Indigenous people aged 25-49 years were hospitalised at a rate 14.2 times higher than that of other people. Hospitalisation rates for pneumococcal pneumonia (not identified as IPD) were more than twice those for IPD for Indigenous adults and almost four times as high for Indigenous people aged 50 years and older, indicating the overall burden of pneumococcal disease among Indigenous people is higher for adults and older people than for infants and young children.
Regional data and national data after 2001 reveal that vaccination programs have had a significant impact on the incidence of IPD among both the Indigenous and non-Indigenous populations . Vaccination has reduced the overall burden of IPD in Australia, but the number of cases of non-vaccine type disease has increased, particularly among non-Indigenous children . The 58% increase between 2002 and 2010 in IPD notifications among Indigenous adults aged 50 years and over has raised concerns that the adult vaccination program may be less than adequate .
The notification rate of IPD for Indigenous children aged less than 2 years (219 per 100,000) at the start of the national Indigenous childhood pneumococcal vaccination program in 2001 was 2.9 times the rate for non-Indigenous children . By 2004, rates for Indigenous children under 2 years had decreased to 92 per 100,000, similar to that for non-Indigenous children . Since the start of the universal childhood pneumococcal vaccination program in 2005, rates have remained relatively stable among Indigenous children but have decreased dramatically for non-Indigenous children : in 2007-2010, the rate of IPD for Indigenous children aged 0-4 years was 2.9 times higher than that for other children . Reflecting the wide distribution of serotypes of IPD among Indigenous people, new vaccines with wider coverage of serotypes would be required to remove the IPD gap between Indigenous and non-Indigenous people.
In 2006-2010, of the 575 reported deaths from IPD for people living in NSW, NT, Qld, SA and WA, 34 (6%) were identified as Indigenous . In children under 5 years of age, there were 30 deaths notified; five (17%) of which were of Indigenous children.
Meningococcal disease is caused by the bacterium Neisseria meningitidis (also known as meningococcus) . Manifestations of meningococcal disease include meningitis, bacteraemia without meningitis, pneumonia and septic arthritis. Meningococcus often causes serious disease that progresses swiftly, with fatality rates of 10-15%; those who survive have a 10-20% probability of lasting sequelae. Meningococcal disease is more common in infants and young children . Possible risk factors for the disease include living in crowded housing conditions, exposure to smokers, recent illness and multiple kissing partners .
The most common groups of meningococcus found in Australia are B and C, with B responsible for most disease in both Indigenous and other people . Vaccination against serogroup C was funded nationally for all infants from 2003; a catch-up program for all people aged up to 19 years ended in 2007 . Vaccination has reduced the burden of serogroup C meningococcal disease in Australia, but there is no vaccination program for serogroup B . A newly licensed vaccination for this serogroup has the potential to reduce the gap in meningococcal disease between Indigenous and other Australians.
Notification rates for both serogroups of meningococcal disease are higher for Indigenous people than for other Australians . In 2007-2010, 104 (10%) of the 1,079 cases of meningococcal disease notified in all jurisdictions were identified as Indigenous. Around one-third (36%) of all cases, and 60% of cases identified as Indigenous, occurred among children aged 0-4 years; rates generally decreased with age for both Indigenous and non-Indigenous people. The average annual age-specific rate of 23 per 100,000 for Indigenous children aged 0-4 years was 3.8 times that for their non-Indigenous counterparts; the rate for Indigenous children aged 5-14 years was 4.1 times higher than that for other children. After age-adjustment, the overall rate for Indigenous people was 2.7 times that of other Australians.
Of the 2,230 recorded hospitalisations for meningococcal disease for people living in NSW, NT, Qld, SA, Vic and WA in 2005-10, 189 (9%) were identified as Indigenous . Over one-third (37%) of all cases, and 67% of cases identified as Indigenous, occurred among children aged 0-4 years. After age-adjustment, the hospitalisation rate for meningococcal disease was 2.2 times higher for Indigenous people than that for non-Indigenous people. Average annual age-specific rates for Indigenous people were highest in the 0-4 years’ age-group (41 per 100,000); a rate 3.5 times higher than that for other children.
There were 42 deaths from meningococcal infection for people living in NSW, NT, Qld, SA and WA in 2006-2010 . Among Indigenous people, up to four deaths30 occurred in the 0-4 years and 5-49 years age-groups; no deaths were recorded for those aged 50 years and older.
Sexually transmissible infections (STIs) are infections that are spread primarily by heterosexual or homosexual contact with an infected person . 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 . 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  .
The majority of STIs are asymptomatic or produce only mild symptoms . 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 .
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 .
Human papilloma virus (HPV) and genital herpes are common STIs in Australia, but they are not notifiable diseases . 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 . 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 is caused by the bacterium Neisseria gonorrhoeae . 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 2010-2012, Indigenous people accounted for 59% of gonorrhoea notifications in Qld, WA, SA, and the NT (excluding 14% of notifications for which Indigenous status was not stated) (Derived from ). The crude notification rate was substantially higher for Indigenous people in these jurisdictions than that for their non-Indigenous counterparts (1,028 and 25 per 100,000, respectively). The jurisdictions with the highest rates among Indigenous people were the NT (2,369 per 100,000) and WA (1,371 per 100,000).
In 2012, 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) . In the non-Indigenous population, gonorrhoea was more common among slightly older people, with those aged 20-39 years accounting for 68% 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 3.6 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 .
In 2012, in the Indigenous population the rate of gonorrhoea diagnosis was 43 and 24 times higher than the rate in the non-Indigenous population .
Syphilis, caused by the organism Treponema pallidum, is a complex infection that has four identified stages: primary, secondary, latent, and tertiary . 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 . 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 .
In 2010-2012, 492 (13%) of the 3,169 people newly diagnosed with syphilis were identified as Indigenous (excluding notifications from the ACT and the 6.1% of notifications for which Indigenous status was not stated) (Derived from ). The crude notification rate for Indigenous people was 5.1 times the rate for non-Indigenous people (25 and 4.9 per 100,000, respectively). In the Indigenous population, the jurisdictions with the highest notification rates were Qld (52 per 100,000) and the NT (39 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 2012 . Among non-Indigenous people, 78% of syphilis cases occurred in people aged 20-49 years.
In 2012, the number of syphilis diagnoses in the Indigenous population was similar for males and females (87 and 80, respectively) . A different pattern was observed in the non-Indigenous population with males accounting for 95% of diagnoses (male to female ratio of 19). This suggests differences in modes of transmission for syphilis in the Indigenous and non-Indigenous populations .
The rates of syphilis notifications were highest among Indigenous people living in remote and very remote areas in 2012, with rates 83 and 64 times those of their non-Indigenous counterparts . Notification rates for non-Indigenous people were highest in major cities.
Chlamydia is caused by the bacterium Chlamydia trachomatis . 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 , but when considering only the jurisdictions with reasonable Indigenous identification31 it is second to gonorrhoea .
Chlamydia was the most reported notifiable disease in Australia in 2010-2012 . Indigenous people accounted for 19% of the notifications of chlamydia in WA, SA, Tas and the NT in 2010-2012 (based on 44,604 cases for which Indigenous status was known) (Derived from ). The crude notification rate for chlamydia was considerably higher for Indigenous people than that for non-Indigenous people (1,566 per 100,000 compared with 328 per 100,000). The highest rate of chlamydia notifications was for Indigenous people living in the NT (671 per 100,000).
Chlamydia is typically diagnosed among adolescents and young adults in both the Indigenous and non-Indigenous populations . In 2012, people aged 15-29 years accounted for around 80% of chlamydia notifications in both populations.
For both the Indigenous and non-Indigenous populations, females accounted for a greater proportion of chlamydia diagnoses than did males in 2012 (65% and 61% of the diagnoses, respectively) . The female to male ratio was 1.8 for Indigenous people and 1.6 for non-Indigenous people.
Indigenous people living in outer regional, remote and very remote areas had the highest rates of chlamydia diagnoses in 2012 . For non-Indigenous people, notification rates in 2012 did not vary much across all geographical areas.
The human immunodeficiency virus (HIV) is a retrovirus that destroys cells in the body’s immune system . Untreated, the virus weakens immune system functioning to the point where minor infections may become fatal . 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 .
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 . 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).
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’ (, 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 .
National surveillance data show that in 2012 there were 1,253 cases of newly diagnosed HIV infection of which 32 (2.6%) were among Indigenous people . Age-standardised rates of HIV diagnosis were similar for Indigenous and non-Indigenous people at 5.5 and 5.4 per 100,000 respectively . Prior to this period, there was a marginal increase in the rate of HIV diagnosis among Indigenous people from around 4.5 per 100,000 in 2003 to 5.5 per 100,000 in 2012. In this period, a nominal increase was also observed in the diagnosis rate among non-Indigenous people. Overall in Australia, the cumulative number of HIV diagnoses by the end of 2012 was 34,029, of which 225 were among Indigenous people .
In 2012, males accounted for 81% of new HIV cases among Indigenous people . The median age of diagnosis for Indigenous males was 27 years.
In comparison, non-Indigenous males accounted for a larger proportion of new HIV cases among non-Indigenous people (81%), and the median age of diagnosis among non-Indigenous males was 36 years (Derived from ).
Three quarters of new HIV infections among the Indigenous population in 2012 were reported in Qld (41%) and NSW (34%) . Indigenous people living in major cities had the highest rates of new HIV diagnoses, 12 per 100,000. The patterns of new HIV infections are slightly different for Indigenous and non-Indigenous people (Derived from ). Most new cases of HIV infections among non-Indigenous people in 2012 were reported in NSW (37%), Vic (25%) and Qld (21%). Among the non-Indigenous population, those residing in major cities had the highest rate of HIV infection (7 per 100,000) . The rates of diagnosis were much lower for the remaining areas of residence, ranging from 2 to 3 per 100,000.
In terms of exposure to HIV, men who have sex with men accounted for over two-thirds (71%) of new HIV cases among Indigenous people in 2012 . Heterosexual contact was also identified as a common form of exposure to HIV among Indigenous people (19%). The percentage of new HIV cases attributed to injecting drug use decreased substantially from 2010 to 2011, with just 4.5% of new HIV cases coming from injecting drug use in 2011 compared with 20% in 2010; rates then rose to 6.5% in 2012. Among non-Indigenous people, 94% of all new HIV cases in 2012 were attributed to the categories ‘men who have sex with men’ (70%) and ‘heterosexual contact’ (24%) (Derived from ). Injecting drug use was responsible for 2.3% of new cases among non-Indigenous people.
Information about the occurrence of AIDS in the Indigenous population in 2012 is not available, but the number of new AIDS cases for the total population in 2009 was only 90 . 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) . The absence of reporting by Indigenous status in the most recent AIDS data  may be due to the marked decrease in new AIDS diagnoses and deaths in Australia over the past decade.
Susceptibility to skin infections and infestations increases with poor living conditions and overcrowding . The significant public health problem posed by skin infections in many remote Indigenous communities, particularly among Indigenous children, requires appropriate education, improved hygiene and reduced overcrowding .
Scabies is a skin disease caused by the mite Sarcoptes scabiei and produces skin inflammation and itching . It is endemic in some remote central and northern Indigenous communities, with prevalence of up to 50% in children  and up to 25% in adults . The East Arnhem regional healthy skin program reported that more than 70% of children had presented to the clinic with scabies at least once in the period 2002-2005, almost all before they reached 2 years of age . 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 .
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 . A study of a remote community in the NT in 2007 found that 82% of children had presented with pyoderma in their first year of life and 87% in their first two years . The pyoderma in Indigenous communities commonly involves group A streptococcus (GAS), which is responsible for continuing outbreaks of acute post-streptococcal glomerulonephritis and ARF .
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 .
A review of non-infectious skin diseases in Indigenous people found the prevalences of psoriasis, type 1 hypersensitivity reactions, and skin cancer were lower than among non-Indigenous people, but the levels of lupus and kava dermopathy higher .
Skin conditions can be linked to serious complications, which can result in hospitalisation and, very uncommonly, death. ICD ‘Diseases of the skin and subcutaneous tissue’ was responsible for 7,994 hospital separations among Indigenous people nationally in 2011-12, accounting for 3.9% of all Indigenous hospitalisations (excluding those from dialysis) . After age-adjustment, the separation rate was 2.5 times higher for Indigenous people than that for 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 children . An analysis of admissions to the Alice Springs Hospital in 2003-2006 found the mean annual incidence rate of Staphylococcus aureus bacteraemia (SAB) was around 20 times higher for Indigenous people than that for non-Indigenous people (161 per 100,000 compared with 8.1 per 100,000) . SAB was community-acquired in over 70% of cases, with skin infections being more common among Indigenous people than among non-Indigenous people.