Communicable disease

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Communicable diseases

Communicable diseases of particular importance to Indigenous people include: tuberculosis; hepatitis (A, B, and C); sexually transmitted infections; HIV/AIDS; Haemophilus influenza type b (Hib); pneumococcal disease, and meningococcal disease [1][2].

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) [3][4]. 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 [4]. 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 [3].

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 inhaling the bacterium Mycobacterium tuberculosis [5]. The bacterium can penetrate the lung’s tissue and start to multiply, potentially causing a variety of symptoms including coughing, weight loss, loss of appetite, fever, chills, as well as the coughing up of blood or sputum. The main risk factors for TB are poverty, overcrowding, and malnutrition [6][7], all common among 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 832 notifications of TB among Australian-born people in Australia in 2003-2007, 172 (21%) were identified as being Indigenous (Derived from [9][10][11][12][13]). Almost one-half (47%) of the new cases among Indigenous people were reported in the NT (80 cases), and one-quarter (25%) in Qld (43 cases) (Table 25). The Australia-wide crude incidence rate of 7.0 cases per 100,000 population for Indigenous people was more than 10 times the rate of 0.7 per 100,000 for non-Indigenous people. The crude incidence rate was highest for the NT (27 cases per 100,000 population).

Table 25: Numbers of new cases and crude notification rates of tuberculosis, Indigenous people, by jurisdiction, Australia, 2003-2007

Jurisdiction	Number	Population	Rate
Source: Derived from Li, 2004 [9], Roche, 2006 [10], Roche, 2007 [11], Roche, 2008 [12] and Barry, 2009 [13]
Notes: Population figures are for 30 June 2004 (the mid-point of the five-year period, 2002-2006) Rates are crude incidence rates per 100,000 population
NSW	22	141,824	3.2
Vic	4	30,329	2.6
Qld	43	136,754	6.3
WA	11	70,945	3.1
SA	9	27,578	6.5
Tas	2	18,333	2.2
ACT	0	4,300	-
NT	80	60,373	26.5
Australia	172	492,677	7.0

The comparison of crude incidence rates underestimates the true difference between Indigenous and non-Indigenous people because of differences in the age structures of the Indigenous and non-Indigenous populations - after adjusting for these differences, the incidence rate for Indigenous people was almost 15 times that of non-Indigenous people (Table 26) (Derived from [9][10][11][12][13]). The incidence of TB was higher for Indigenous people than for non-Indigenous people across all age-groups, with rate ratios being highest for the 45-54 years and 55-64 years age-groups.

Table 26: Numbers of new cases and notification rates of tuberculosis, by Indigenous status and age-group, and Indigenous:non-Indigenous rate ratios, Australia, 2003-2007

Age group	Indigenous		Non-Indigenous		Rate ratio
Number	Rate	Number	Rate
Source: Derived from: Li, 2004 [9], Roche, 2006 [10], Roche, 2007 [11], Roche, 2008 [12] and Barry, 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 incidence 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	10	3.3	44	0.7	4.5
5-14	10	1.6	41	0.3	5.2
15-24	22	4.5	42	0.3	14.5
25-34	32	8.7	68	0.5	18.0
35-44	26	8.4	49	0.3	25.3
45-54	33	16.0	72	0.5	30.6
55-64	19	17.5	67	0.6	28.4
65+	20	29.4	277	2.1	14.1
All ages	172		660		14.8

Hepatitis

Hepatitis, an inflammation of the liver, can be caused by viral infections, alcohol or drug misuse, other toxins, or an attack by the body’s immune system on itself [14]. The viruses identified most frequently have been designated hepatitis A, B, and C (hepatitis types D through G have been identified also). 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) [15][16]. HAV is often asymptomatic among young children, but, among older people, symptoms may include fever, fatigue, nausea, diarrhoea, jaundice, and vomiting. Death due to HAV is very rare.

Of the 179 notifications of HAV for people living in WA, SA, and the NT in 2008-2010, 3 (1.7%) were identified as being Indigenous (Derived from [17][18][19][20][21]). The crude notification rate of 0.9 per 100,000 for Indigenous people was slightly less than the rate of 1.1 per 100,000 for non-Indigenous people.

It is likely that the low levels of HAV infection, particularly among Indigenous people, reflect the introduction of hepatitis A 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) [15]. There has not been a notified case of HAV among Indigenous people in the NT since 2006 (there have been 9 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 the north 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 [16][23][24].

Of the 162 notifications of HBV for people living in WA, SA, and the NT in 2008-2010, 9 (5.6%) were identified as being Indigenous (Indigenous status was not stated in 1.9% of cases) (Derived from [17][18][19][20][21]). The crude notification rate of 2.7 per 100,000 for Indigenous people was 2.2 times the rate of 1.3 per 100,000 for non-Indigenous people.

For the Indigenous population, the rate of HBV diagnoses in 2010 was highest among those aged 30-39 years [18]. Indigenous people had a considerably higher rate of HBV diagnoses in almost every age-group. Indigenous males were 1.7 times more likely to be diagnosed with HBV than were Indigenous females.

Major cities, very remote, and outer regional areas had the highest rates of newly acquired HBV infection in the Indigenous population [18]. The rate of infection was highest for non-Indigenous people in major cities.

A vaccination program commencing in Indigenous communities in the mid-1980s has had considerable success [25], but some studies suggest that Indigenous children had a sub-optimal response to the HBV vaccine more often than their non-Indigenous counterparts [26][27]. Possible explanations for the inefficiency of the vaccine include a failure in the cold-chain (maintaining the vaccine within a sufficiently cool temperature range), genetic differences, or extrinsic environmental factors, such as heavy smoking 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 in the Indigenous community [25].

Hepatitis C

Transmission of hepatitis C virus (HCV) typically occurs via blood-to-blood contact [28]. Injecting drug use (IDU) 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 [16]. 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, while 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].

Of the 5,784 notifications of HCV for people living in WA, SA, and the NT in 2008-2010, 645 (11%) were identified as Indigenous (8.6% of notifications did not state Indigenous status) (Derived from [17][18][19][20][21]). The crude notification rate of 197 per 100,000 for Indigenous people was 5.1 times the rate of 39 per 100,000 for non-Indigenous people. Over the five-year period 2006 to 2010, notification rates were consistently much lower for Indigenous people living in the NT than for those living in WA and SA [18].

In contrast to other reported communicable diseases, the rate of newly diagnosed HCV infection among Indigenous persons was highest for those living in inner regional areas and major cities [18]. For non-Indigenous people, the rates for those living in remote and very remote areas were slightly higher than for those living in major cities and inner and outer regional areas.

The age pattern of newly diagnosed HCV was slightly different for the Indigenous and non-Indigenous populations [18]. Among Indigenous people, rates were highest for those in the 20-29 years, 30-39 years, and 40-49 years age-groups. For non-Indigenous people, they were highest in the 30-39 years, 40-49 years, and 50-59 years age-groups. Rates were generally higher for males than for females for both populations.

Haemophilus influenzae type b

Haemophilus influenza type b (Hib) is a bacterium that can cause meningitis, epiglottitis, pneumonia, septicaemia, cellulitis, osteomyelitis, pericarditis and septic arthritis [31]. Babies and children are particularly susceptible to Hib, 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 [32].

Extent of Hib disease among Indigenous people

Hib notifications in Australia declined steeply following the commencement of nationally-funded infant vaccination in 1993, but the disease persists at much lower levels [33]. Hib notifications in Australia declined from 617 cases reported in 1993-1994 to 32 cases in 2004-2005, with no deaths during 2005 [34].

The incidence of invasive Hib disease has declined sharply, but Indigenous populations continue to be at higher risk of contracting Hib than are non-Indigenous populations [34]. In 2004-2005, Indigenous people were 7.5 times more likely than non-Indigenous people to be diagnosed with invasive Hib. This ratio is lower than in 2002-2003 (17.5), but much higher than the pre-vaccination ratio of 2.7 in 1993-1994. Similarly, in 2003-2006, Indigenous people were 8.8 times more likely to contract Hib than their non-Indigenous counterparts [33].

Pneumococcal disease

Pneumococcal disease, which is caused by the bacterium Streptococcus pneumonia (pneumococcus), normally includes upper respiratory tract and lower respiratory tract infection (primarily pneumonia) [35]. Invasive pneumococcal disease (IPD) occurs when the bacterium infects normally sterile sites, such as blood and cerebrospinal fluid, causing life-threatening septicaemia and meningitis. Recognised risk factors for pneumococcal disease include chronic illness (including chronic respiratory, cardiac and renal diseases) and immuno-compromised conditions [36][37]. Children aged less than five years are particularly susceptible to pneumococcal disease [38].

Vaccination for pneumococcal disease became available in 1999 for Indigenous adults aged 50 years and older and Indigenous people aged 15-49 years with high-risk conditions [35]. In 2001, nationally-funded vaccination became available for Indigenous infants and young children and for all Australian children with high-risk conditions. From 2005, vaccination has been funded for all Australian infants and for all people aged 65 years and older [35][36].

Extent of pneumococcal disease among Indigenous people

Indigenous children and adults have a significantly higher incidence of pneumococcal disease than do non-Indigenous people, but detailed data are available only for IPD [37], which has been notifiable Australia-wide since 2001 [36].

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 more than seven times higher than the rate for other people (6.3 per 100,000) ¹⁴ [39]. For Indigenous people, notification rates were highest in the 65 years and older age-group (114 compared with 17 per 100,000) and in the 45-54 years age-group (58 compared with 5.1 per 100,000). Importantly, the incidence for Indigenous people aged 35-44 years and 45-54 years was very high, with rates (50 and 58 per 100,000, respectively) almost 12 times higher than those for other people (4.3 and 5.1 per 100,000, respectively).

Vaccination programs have had a significant impact on the number of cases of IPD among both Indigenous and non-Indigenous people, but notification rates remain higher for Indigenous people than for non-Indigenous people [40][41]. At the start of the national Indigenous childhood pneumococcal vaccination program in 2001, the rate for Indigenous children aged less than two years (219 per 100,000) was 2.9 times higher than the rate for non-Indigenous children (75 per 100,000) [41]. By 2004, rates for Indigenous and non-Indigenous children under two years were similar (92 and 94 per 100,000, respectively); since that time the rates have remained relatively stable among Indigenous children, but decreased for non-Indigenous children, leading to an increasing gap. There is no current information on children under two years, but Indigenous children 0-4 years had 3.7 times the rate of notification of other children in 2006-2008 [39].

For Indigenous adults, IPD rates decreased after the introduction of vaccination programs in the Kimberley, WA [42] and in north Qld [43], but rates remain higher for Indigenous adults than for non-Indigenous adults nationally [36]. The high rates of IPD notifications for Indigenous people are reflected in hospitalisation rates for pneumococcal septicaemia and meningitis [33].

In terms of mortality, two (19%) of the 11 deaths from IPD for people living in Qld, WA, SA and the NT in 2003-2005 were identified as Indigenous [33].

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 [44]. In 2009, the most common groups of meningococcus found in Australia were B (88%) and C (5.9%), with proportions similar to those in 2007 and 2008 [45]. Vaccination against serogroup C was funded for all infants from 2003: a catch-up program for all people aged up to 19 years of age ended in 2007.

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 five years are particularly susceptible [33]. Previously recorded outbreaks among Indigenous children north-west Qld were due to serogroup C [46], but the disease in young children is now mainly due to serogroup B [47].

In 2003-2006, 8.4% (106 cases) of the 1,263 cases of meningococcal disease notified in NSW, Vic, WA, SA and the NT were identified as Indigenous [33]. More than 32% of all cases and almost 69% of cases identified as Indigenous occurred among children 0-4 years. The rate of 45 per 100,000 for Indigenous children aged 0-4 years was 4.9 times the rate of 9.2 per 100,000 for their non-Indigenous counterparts. Across all age-groups, the age standardised rate of 5.1 per 100,000 for Indigenous people was more than twice the rate of 1.9 per 100,000 for other Australians.

There were 21 deaths from meningococcal disease for people living in Qld, WA, SA and the NT in 2003-2005 [33]. 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 [48]. 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 teenagers and young adults, and unprotected sex is generally the primary risk factor [49].

The majority of STIs are asymptomatic or produce only mild symptoms [1][49]. Many people affected find out they have an infection through screening and contact tracing [1]. 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 [50][51].

The NNDSS collects data on some STIs, including chlamydia, gonorrhoea, syphilis, donovanosis, and HIV/AIDS [3]. 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 [52]. Variations in notification rates over time may reflect real changes in incidence, but could also be due to the introduction of easier and more sensitive testing procedures, greater targeted screening, and public awareness campaigns [53]. The high screening rates in some Indigenous communities probably contributes to the higher rates reported for Indigenous people than for non-Indigenous people [50][54].

Gonorrhoea

Gonorrhoea is caused by the bacterium Neisseria gonorrhoeae [55]. 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. In some instances, untreated gonorrhoea can lead to infertility in both women and men.

For people living in Qld, WA, SA and the NT, notification rates of gonorrhoea were much higher for Indigenous people than for non-Indigenous people in the three-year period 2008-2010: 1,244 cases per 100,000 population (based on 9,919 cases notified) compared with 25 per 100,000 (based on 6,088 cases notified) (Derived from [17][18][21]). (These rates do not include the 13% of notifications for which Indigenous status was not stated.) The highest rates for Indigenous people were for the NT (32,783 per 100,000) and WA (3,334 per 100,000). Notification rates for gonorrhoea increased slightly for both Indigenous and non-Indigenous people over the five-year period 2006-2010.

In 2010, gonorrhoea notification rates were highest for Indigenous people aged 15-19 years and 20-29 years [56]. For non-Indigenous people, the rates were highest in the 20-29 years and 30-39 years age-groups. The number of notifications of gonorrhoea in 2010 was slightly higher for females than males among Indigenous people, but males contributed 78% of the notifications for non-Indigenous people [18].

In 2006-2010, gonorrhoea notification rates were much higher for Indigenous people living in remote and very remote areas than for those living in major cities and inner and outer regional areas [18]. For non-Indigenous people, notification rates were also highest in very remote and remote areas.

Syphilis

Syphilis, caused by the organism Treponema pallidum, is a complex infection that has four identified stages: primary, secondary, latent, and tertiary [57]. 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 [56]. 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 [58].

Australia-wide, notification rates of syphilis were much higher for Indigenous people than for non-Indigenous people in the three-year period 2008-2010: 27 per 100,000 (based on 439 cases notified) compared with 5.1 per 100,000 (based on 3,249 cases notified) (Derived from [17][18][21]). (These rates do not include the 4.4% of notifications for which Indigenous status was not stated.) More than nine-tenths (93%) of the Indigenous notifications were for Qld, WA, SA and the NT, for which jurisdictions the notification rate for Indigenous people (51 per 100,000) was 15 times the rate for non-Indigenous people (3.3 per 100,000).

Australia-wide, syphilis notification rates decreased for Indigenous people from 40 per 100,000 in 2006 to 25 per 100,000 in 2010 [18]. Notification rates increased for non-Indigenous people from 3 per 100,000 in 2006 to 5 per 100,000 in 2010.

Syphilis notification rates in 2010 were highest among Indigenous people aged 20-29 years [56]. Among non-Indigenous people, the rate was highest in the 30-39 years age-group. Indigenous males accounted for 61% of the notifications of syphilis among Indigenous people in 2010; males contributed 94% of the notifications among non-Indigenous people [18].

Syphilis notification rates were much higher for Indigenous people living in remote and very remote areas than for those living in major cities and inner and outer regional areas [18]. For non-Indigenous people, notification rates were highest in major cities and in very remote areas.

Chlamydia

Chlamydia, caused by the bacterium Chlamydia trachomatis, is the most common STI among Indigenous people in Australia [50][59]. The infection in women can cause cervicitis, endometritis, and pelvic inflammatory disease, which can lead to tubal factor infertility and ectopic pregnancy [59]. In men, it can cause urethritis, epididymo-orchitis, and prostatitis. Due to lack of obvious symptoms of the disease, the incidence of chlamydia is underestimated in notification data.

Notification rates for chlamydia were much higher for Indigenous people living in WA, SA and the NT in the three-year period 2008-2010 than for their non-Indigenous counterparts: 2,726 per 100,000 (based on 8,936 cases notified) compared with 314 per 100,000 (37,537 cases notified) (Derived from [17][18][21]). (These rates do not include the 14% of notifications for which Indigenous status was not stated.) Notifications of chlamydia for Indigenous people increased between 2008 and 2010, but the increase was not as great as for non-Indigenous people.

For both Indigenous and non-Indigenous people, notification rates of chlamydia in 2010 were highest for people aged 15-29 years, and higher for females than for males [56]. Notification rates for Indigenous people were much higher in remote and very remote areas than in major cities and inner and outer regional areas [18]. Among non-Indigenous people, notification rates were slightly higher for remote and very remote areas but similar for the other areas.

HIV/AIDS

The human immunodeficiency virus (HIV) is a retrovirus that destroys cells in the body’s immune system [56]. 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 antiretroviral 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 [60]. The behaviour that presents the greatest risk of exposure to HIV is unprotected anal sex. Other unsafe 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 [3]. 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’ ([61], p.6). Indigenous people are regarded as being at particular risk of HIV infection due to their higher rates of STIs and more limited access to health care services [62].

Extent of HIV/AIDS among Indigenous people

National surveillance data show the number of newly diagnosed HIV infections in the Indigenous population were almost the same in 2009 and in 2010 (23 and 22 new cases, respectively) [18]. Over the decade 2001-2010, the number of new HIV diagnoses among Indigenous people increased by 57% (14 new cases in 2001), but a year-by-year analysis shows fluctuations in the number of new cases. In 2010, males accounted for 68% of Indigenous HIV diagnoses . The median age of Indigenous people newly diagnosed with HIV was 35 years.

In comparison, new diagnoses of HIV in the non-Indigenous population decreased slightly from 2009 to 2010 (1,039 and 1,021 cases, respectively) (Derived from [18]). Males accounted for 86% of new HIV diagnoses in the non-Indigenous population and the median age of diagnosis among non-Indigenous people was 36 years.

Around two-thirds of new HIV infections among the Indigenous population in 2010 were reported in Qld (36%), and NSW (32%) [18]. In terms of exposure to HIV, men who have sex with men accounted for almost two-thirds (60%) of new HIV cases among Indigenous people. Injecting drug use and heterosexual contact were also identified as common exposures to HIV among Indigenous people (20% and 15%, respectively). The majority of new Indigenous HIV infections occurred in major cities; the rate of infection generally declined as the area of residence became more remote.

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 2010 were reported in NSW (34%). Vic (27%) and Qld (23%) also accounted for substantial proportions of the new cases. Among non-Indigenous people, 94% of all new cases in 2010 were attributed to the categories ‘men who have sex with men’ (66%) and ‘heterosexual contact’ (28%). Injecting drug use was responsible for only 2.0% of new cases among non-Indigenous people.

Overall in Australia, the cumulative number of HIV diagnoses by the end of 2010 was 30,486, of which 207 were among Indigenous people [18].

Information about the occurrence of AIDS in the Indigenous population in 2010 is not available, but the number of new AIDS cases for the total population in 2009 was only 90 [19]. 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) [63]. The absence of Indigenous status in the most recent AIDS data [19] 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 increase with poor living conditions and overcrowding [64][65]. Skin infections in many Indigenous communities reflect serious health inequalities, but have attracted much less professional attention than they deserve [66]. Scabies, a disease caused by the mite Sarcoptes scabiei resulting in inflammation and itching [67], is endemic in some remote central and northern Indigenous communities, with prevalence up to 50% in children [68] and up to 25% in adults [69]. 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 [70]. 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 [71].

Scratching in response to the inflammation and itching of scabies infestation can result in pyoderma (also referred to as impetigo), a bacterial infection of the skin that can lead to kidney disease and possibly heart disease [72]. 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 [71]. The pyoderma in Indigenous communities commonly involves group A streptococcus (GAS), which is responsible for continuing outbreaks of post-streptococcal glomerulonephritis and acute rheumatic fever [72][73].

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 [72].

Skin conditions can be linked with serious complications, which can result in hospitalisation and, very uncommonly, death. The most current detailed information about hospitalisation for skin conditions among Indigenous people is for June 2006 to July 2008, during which period they accounted for around 3.9% of hospital admissions (excluding dialysis) of Indigenous people in NSW, Vic, Qld, WA, SA and the NT, at 2.3 times the rate of other people [39].

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Endnote

14. Indigenous rates have been compared with those for all other people, including those for whom Indigenous status was not known.

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