Communicable diseases

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

For 2000-01, the Indigenous hospitalisation rate for communicable diseases including infectious and parasitic diseases was more than twice that of non-Indigenous people [3]. The highest rates of hospital separations for ‘infectious and parasitic diseases’ occurred in Indigenous children less than one year of age followed by those aged 1-4 years.

Risk factors for communicable diseases vary according to type of disease. Communicable diseases can be caused by: bacteria (for example, pertussis (whooping cough) and tuberculosis); bacterial toxins (for example, some forms of food poisoning); viruses (for example, measles, influenza and HIV); fungi (for example, tinea); protozoan parasites (for example, malaria) [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.

Information regarding specific communicable diseases comes from a variety of sources, including individual studies and State and Territory based notifiable disease collections. Data from State 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.

Tuberculosis

Tuberculosis is primarily a lung infection caused by the bacterium Mycobacterium tuberculosis, which penetrates the lung tissue, causing inflammation and the development of encapsulated bacterial cells (tubercles) [5]. The main risk factors for tuberculosis 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 abuse, and advanced renal disease. A recently emerged risk factor for tuberculosis is HIV [8].

Extent of tuberculosis among Indigenous people
Of the 570 notifications of tuberculosis among Australian-born people in Australia in 2001-2003, 117 (20.5%) were identified as being Indigenous [derived from 9, 10, 11]. The crude notification rate of 8.4 per 100,000 for Indigenous people was almost 11 times the rate of 0.8 per 100,000 for other Australian-born people. After adjusting for the differences in the age structures of the Indigenous and other Australian-born populations, the incidence rate for Indigenous people was 15 times that of other Australian-born people.

Given that 86% of Indigenous cases in 2001-2003 occurred among people living in Queensland, WA, or the NT [derived from 9, 10, 11], an analysis restricted to those jurisdictions would probably reveal even greater differences between Indigenous and other Australian-born people. (Such an analysis was not possible as the published sources did not include the necessary data.)

Hepatitis

Hepatitis, an inflammation of the liver, can be caused by viral infections, alcohol or drug abuse, 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 been identified also).

Hepatitis A
Of the 1,012 notifications of hepatitis A for people living in NSW, WA, SA, and the NT in 2000-2002, 113 (11%) were identified as being Indigenous [12]. The standardised notification rate of 9.1 per 100,000 for Indigenous people was almost three times the rate of 3.1 per 100,000 for other people. Differences between Indigenous and other people in notification rates were particularly high among children, with rate ratios of 22 for the 0-4 years age group and 7.7 for the 5-14 years age group.

The real incidence of hepatitis A among Indigenous people is probably much higher than these figures suggest, however, as the disease is endemic in many rural and remote communities [13,14].

Hepatitis B
Of the 526 notifications of hepatitis B for people living in NSW, WA, SA, and the NT in 2000-2002, 57 (11%) were identified as being Indigenous [12]. The standardised notification rate of 7.2 per 100,000 for Indigenous people was more than four times the rate of 1.6 per 100,000 for other people. Notification rates were highest in the 15-24 years and 25-49 years age groups for both Indigenous and other people, but the difference in rates was greatest for people aged 50 years or older.

The relatively few notifications among people aged less than 15 years (3 Indigenous and 13 others) probably reflect the impact of childhood hepatitis B vaccination programs, which were first introduced for Indigenous people in the NT in the 1980s [12, 15]. These programs appear to have changed the incidence pattern of hepatitis B among Indigenous people, as early research suggests that the virus had been present at high levels in some Indigenous populations for some time: the virus was originally known as the ‘Australia antigen’ after its discovery in an Australian Aboriginal person in 1965 [16].1 With a high prevalence in some Indigenous populations, transmission may have occurred more from mother to baby and horizontally through infected wounds on the surface of the skin, rather than its current modes: via blood (particularly from contaminated injecting equipment) and sexually.

Hepatitis C
Of the 11,855 notifications of hepatitis C for people living in WA, SA, and the NT in 1999-2003, 793 (7%) were identified as being Indigenous (in 34% of notifications, Indigenous status was not stated) [Derived from 17]. The crude notification rate of 107 per 100,000 for Indigenous people was almost three times the rate of 39 per 100,000 for other people.

Because of the large proportions of notifications in which Indigenous status was not stated, these rates are likely to under-estimate the true difference between Indigenous and non-Indigenous people in notifications of hepatitis C. SA is the only jurisdiction with very low levels of ‘not stated’ notifications (3.2% for 1999-2003). The extent to which the situation in SA applies to other jurisdictions is not known, but 328 (8%) of the 4,011 notifications of hepatitis C in that State in 1999-2003 were identified as Indigenous. The crude notification rate of 257 per 100,000 for Indigenous people was almost seven times the rate of 38 per 100,000 for non-Indigenous people.

Infection with hepatitis C virus (HCV) occurs via contact with contaminated blood – typically through sharing of a needle during IV drug use (suspected in 75% of new cases), tattooing, or a blood transfusion [18]. HCV can also be passed from mother to foetus during pregnancy. Conflicting reports exist, but sexual contact may be another potential route of transmission. No vaccine exists for HCV. Preventive measures include avoiding IV drug use.

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 [19]. 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 [20].

Hib notifications in Australia declined steeply following implementation of the national vaccination strategy in 1993, but the disease persists at much lower levels [4]. Hib notifications in Australia declined from 533 cases reported in 1991 to 29 cases in 2002, with only two deaths recorded in 2002. However, of 47 notifications of invasive Hib in 2000-2002 in jurisdictions with adequate data, 24 were for children 0-4 years and, of these, 11 (46%) were Aboriginal and/or Torres Strait Islander children [12]. Among children aged 0-4 years, the annual notification rate for Aboriginal and Torres Strait Islander children was 10 per 100,000 compared with 0.7 per 100,000 for other children. (These rates represent a reduction of almost 98% since vaccination was introduced.)

Pneumococcal disease

Pneumococcal disease, which is caused by the bacterium Streptococcus pneumoniae (pneumococcus), includes upper respiratory tract infection and lower respiratory tract infection (primarily pneumonia) [2, 12]. 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. Children aged less than five years are particularly susceptible to pneumococcal disease.

Extent of pneumococcal disease among Indigenous people
Indigenous children and adults have a significantly higher incidence of pneumococcal disease than non-Indigenous people, but detailed data are available only for IPD, which has been notifiable Australia-wide since 2001 (since 1997 in Queensland and the NT) [2, 12].

Based on notifications for people living in NSW, NT, WA and SA in 2001-2002, the incidence of IPD among Indigenous people (45 per 100,000) was 4.5 times that among other people (10 per 100,000) [12].2 For both Indigenous and other people, notification rates were highest in the 0-4 years age group (87 per 100,000 for Indigenous people and 49 per 100,000 for other people) and in the 50 years and over age group (59 per 100,000 compared with 14 per 100,000). Importantly, the incidence among Indigenous people aged 25-49 years was also very high, with a rate (48 per 100,000) 12 times higher than that among other people (4 per 100,000). These aggregated data conceal important regional differences, with notification rates being much higher for the NT (120 per 100,000 in 2001 and 86 per 100,000 in 2002) [21, 22]. The rate among NT Indigenous children aged less than 5 years was 483 per 100,000 in 2001.

The high rates of IPD notifications among Indigenous people are reflected in hospitalisation rates for pneumococcal septicaemia and meningitis [12]. Of the 21 deaths from IPD for people living in Queensland, WA, SA and the NT in 2000-2002, five (24%) were identified as Indigenous.vii Two of the five deaths identified as Indigenous were of children aged less than 5 years.

Vaccination for IPD is targeted for Indigenous children 0-2 years (except in central Australia and adjacent areas where the conjugate pneumococcal vaccine program extends to five years of age) [12]. Vaccination with the polysaccharide vaccine is recommended for Indigenous adults with risk factors for IPD (all Indigenous adults aged 15 years or over are eligible in the NT), and for all Indigenous people aged 50 years or older.

Meningococcal disease

Meningococcal disease is caused by the bacterium Neisseria meningitidis (also known as meningococcus). Manifestations of meningococcal disease include meningitis, meningococcaemia without meningitis, and septic arthritis [12]. The risk of infection can be increased in crowded housing conditions [23].

Extent of meningococcal disease among Indigenous people
The incidence of meningococcal disease is higher among Indigenous people than other Australians, and children aged less than five years are particularly susceptible [12].

Almost 9% (92 cases) of the 1,067 cases of meningococcal disease notified in NSW, WA, SA and the NT in 2000-2002 were identified as Indigenous. More than 31% of all cases and almost 61% of cases identified as Indigenous occurred among children aged 4 years or younger. The rate of 51 per 100,000 for Indigenous children aged 0-4 years was 3.5 times the rate of 15 per 100,000 for their non-Indigenous counterparts. Overall, the standardised rate of 7.2 per 100,000 for Indigenous people was more than twice the rate of 3.4 per 100,000 for other Australians [12]. These combined rates for NSW, WA, SA and the NT conceal important regional differences in notification rates: in 2001, the crude notification rates were 19.7 per 100,000 for Indigenous people living in WA, and 15.8 per 100,000 for those living in the NT [23].

There were 38 deaths from meningococcal disease for people living in Queensland, WA, SA and the NT in 2000-2002 [12].3 Five of these deaths were of people identified as Indigenous, four of whom were aged 0-4 years.

The most common groups of meningococcus found in Australia are B (60%) and C (34%), with vaccination available only for serogroup C [24]. Previously recorded outbreaks among Indigenous children in central Australia and north-west Queensland were due to types A and C [25], but recent data suggests that the disease in young children is now mainly due to serogroup B.

Sexually transmitted infections

Sexually transmitted infections (STIs) are spread by heterosexual or homosexual contact with an infected person and most cases are found among sexually active teenagers and young adults [1]. Unprotected sex is a main risk factor for STIs. Infections that can be transmitted through sexual contact include gonorrhoea, syphilis, HIV/AIDS, hepatitis B, chlamydia, human papilloma virus (HPV), genital herpes and donovanosis. 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 [26]. Most STIs are asymptomatic or produce mild symptoms, and people affected often find out they have an infection through screening and contact tracing [27]. STIs can usually be effectively treated if diagnosed early, but, if left untreated, they may lead to complications.

Variations in notification rates over time may reflect real changes in incidence, but could be due also to the introduction of easier and more sensitive testing procedures, improved education encouraging notification reports from health authorities, and improved contact tracing [28].

Gonorrhoea

Gonorrhoea, which is caused by the bacterium Neisseria gonorrhoea and mainly affects the mucosal and glandular structures of the genital tract (cervix in women, urethra in men), is highly contagious [29]. It can cause pelvic inflammatory disease in women, which can result in ectopic pregnancy or sterility.

The notification rate of gonorrhoea for Indigenous people living in WA, SA and the NT in 2003 was 1,403 cases per 100,000 population (based on 2,151 cases notified), compared with a rate of 29 per 100,000 (999 cases notified) for non-Indigenous people [17].

The disease can be successfully treated with oral antibiotics, but some strains of N. gonorrhoeae in urban Australia are penicillin-resistant [27]. Ceftriaxone is used as treatment in communities in Queensland, for example, where penicillin resistant strains have been found [30]. People with gonorrhoea often also have chlamydia, so the infections are often treated at the same time.

Syphilis

Syphilis, which is caused by the organism Treponema pallidum, is an STI that has primary, secondary, latent, and tertiary stages [31]. The infection is especially contagious during the primary phase, when sores are present and is generally not contagious during the latent phases. Untreated syphilis can lead to serious damage of the nervous system and other body organs, or to death. Penicillin is the usual treatment [27].
The notification rate of syphilis for Indigenous people living in WA, SA and the NT in 2003 was 303 cases per 100,000 population (based on 381 cases notified), compared with a rate of 3 per 100,000 (100 cases notified) for non-Indigenous people [17].

Chlamydia

Chlamydia, which is caused by the bacterium Chlamydia trachomatis, is one of the most common STIs in Australia [27]. The infection in women can cause cervicitis, endometritis, and pelvic inflammatory disease, leading to tubal factor infertility and ectopic pregnancy. In men, it can cause urethritis, epididymo-orchitis, and prostatitis. Azithromycin treatment for chlamydial infection has been a major advance. Due to lack of obvious symptoms of the disease, incidence is underestimated by notification data.

Notification rates for chlamydia were much higher for Indigenous people living in WA, SA and the NT in 2003 than for their non-Indigenous counterparts: 1,323 cases per 100,000 population (based on 2,049 cases notified) compared with 161 per 100,000 (5,306 cases notified) [17].

HIV / AIDS

Australia has so far successfully prevented an uncontrolled spread of HIV (human immunodeficiency virus) and the overall rates of HIV and AIDS (acquired immune deficiency syndrome) are low in comparison with other countries [32]. 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’ [33]. Indigenous people were seen as being at particular risk of HIV infection due to high rates of STIs and their lack of access to effective services [28].

HIV is transmitted from person to person through the exchange of blood and bodily fluids. In Australia, transmission occurs primarily through sexual contact between men. The virus can also be transmitted through: sexual contact between men and women; sharing of needles and/or syringes (primarily for drug injection) with someone who is infected; and, very rarely in countries like Australia where blood is screened for HIV antibodies, through transfusions of infected blood or blood clotting factors. Babies born to HIV-infected women may become infected before or during birth or through breast-feeding after birth.

HIV/AIDS among Indigenous people
Overall, notification rates for HIV infection and AIDS are similar for the Indigenous population and the non-Indigenous population, and appear to have declined at similar rates over the past decade. For the five-year period 1999-2003, the notification rate for HIV infection was 3.8 cases per 100,000 for both the Indigenous and non-Indigenous populations [17]. These rates are lower than those reported for 1992-1998: 5.2 per 100,000 for Indigenous people and 5.5 per 100,000 for non-Indigenous people [34]. For 1999-2003, the rates of AIDS diagnoses were 1.2 per 100,000 for both the Indigenous and non-Indigenous populations [Derived from 17].

There have been some important differences between Indigenous people and the total population in the characteristics of newly diagnosed HIV infection over the ten-year period 1994-2003 – in terms of age at diagnosis and exposure categories4 [17]. The median age of diagnosis of HIV among Indigenous people was 30 years compared with almost 33 years for the total population. In contrast to the total population, for which less than 8% of diagnoses of HIV occurred in females, more than 31% of cases reported among Indigenous people occurred in females. Infection was acquired by heterosexual contact in 39% of cases among Indigenous people and in only 11% of cases among the total population. Male homosexual contact was responsible for 77% of cases in the total population and for 36% in the Indigenous population, and male homosexual contact with injecting drug use for 4% and almost 11% respectively. Injecting drug use without male homosexual contact was responsible for 4% of cases in the total population and for more than 12% in the Indigenous population.

Overall in Australia, the cumulative number of HIV diagnoses by the end of 2003 after adjustment for reporting delay was estimated to be 20,580 [17]. For the same period, after adjustment for reporting delay, there were 9,380 AIDS cases and 6,372 deaths following AIDS. In comparison, there were 203 HIV notifications among the Indigenous population in the period 1992-2003 and 78 AIDS diagnoses.

Skin infections and infestations

Susceptibility to skin infections increases with poor living conditions and overcrowding [35]. Skin infections and infestations in Indigenous communities reflect serious health inequalities, but have attracted much less professional attention than they deserve. Scabies, a disease caused by the mite Sarcoptes scabiei resulting in inflammation and itching [36], is endemic in many remote Indigenous communities, with prevalence in children up to 50% [35, 37]. The cycles of scabies transmission 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. Up to 70% of children living in some Indigenous communities have skin sores, with group A streptococcus (GAS) the major pathogen [37]. GAS is responsible for continuing outbreaks of post-streptococcal glomerulonephritis and acute rheumatic fever. 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 [36].

Skin diseases cause very few deaths directly, but they can be linked with serious complications. They did, however, account for around 2.5% of hospital separations in 2002-03 for patients identified as Indigenous, at a rate around two-and-a-half times that of non-Indigenous people [38].

Gastroenteritis

Gastrointestinal infections and infestations, particularly those causing diarrhoea, are still significant causes of morbidity among Indigenous children [39].

Diarrhoea, usually referred to as gastroenteritis, is not a major problem among non-Indigenous children in Australia, but it remains a common cause of morbidity for Indigenous children. The greater impact of gastroenteritis among Indigenous than among non-Indigenous children is reflected in hospitalisation data. Unfortunately, detailed data are available only for WA: these data reveal that separation rates for gastroenteritis in the first two years of life are around 10 times higher for Indigenous children than for non-Indigenous children [40]. Separation rates in WA 2000 were 147 per 1,000 for Indigenous infants (less than 12 months of age) and 114 per 1,000 for Indigenous children in their second year of life. Rates for children aged between 2 and 10 years are considerably lower, but the Indigenous:non-Indigenous rate ratios are around 3-4. Separation rates in WA in 2000 were considerably higher for Indigenous infants living outside the Perth metropolitan area (184 per 1,000) than for metropolitan residents (69 per 1,000) [40].

Hospital separation rates for gastroenteritis in WA declined by around 22% between 1994 and 2000 for both Indigenous and non-Indigenous infants [40]. The declines in rates were slightly higher for children in their second year of life: 31% for Indigenous children and 25% for non-Indigenous children. The declines in rates were slightly higher for children living outside the Perth metropolitan area than for metropolitan residents.

Around one-third of 1,001 infants born in WA in 1995 and 1996 who had an index admission for gastroenteritis during their first year of life were Indigenous [41]. Follow-up of this group of infants until 31 May 2002 revealed that 58% of children admitted more than once were Indigenous. Overall, Indigenous children made up more than 38% of all admissions for gastroenteritis. Compared with non-Indigenous children admitted for gastroenteritis, Indigenous children were more likely to: be seriously dehydrated on admission (36% compared with 24%); be undernourished5 (13% compared with 4%); have iron deficiency anaemia (8% compared with 1%); and have gastrointestinal carbohydrate intolerance (10% compared with 5%).

Similar measures of serious illness were documented among children admitted to Royal Darwin Hospital in 1997–98: half of the 44 Indigenous children hospitalised for diarrhoea were acidotic, 32 had moderate to severe hypokalaemia, and 37 had dehydration equivalent to a loss of more than 5% of body weight [42]. Many of the children had an underlying intestinal enteropathy characterised by partial atrophy of the small intestinal villi, which also contributed to gastrointestinal carbohydrate intolerance.

Another expression of the decline in gastroenteritis among Indigenous children, at least in terms of severity, is the marked reductions in mortality. In the period 1970-1979, there were 69 deaths of Indigenous children in hospital in WA from gastroenteritis (53 were infants) [40]. In the period 1980-1989, there were nine Indigenous deaths (six infants), but none in the period 1990-2000.

References

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Endnote

1 See Burns et al., 2003 [1] for details.

2 These jurisdictions are the only ones with reasonable levels of identification of Indigenous people in notifications. Indigenous rates have been compared with those for all other people, including those for whom Indigenous status was not known.

3 Caution needs to be exercised in interpretation of the various death rates presented in this report, most of which are based on the numbers of deaths registered as Indigenous. These numbers underestimate the actual numbers of Indigenous deaths, with the level of underestimation varying by jurisdiction (see ‘Limitations of the sources of Indigenous health information’). The ‘projected’ death rates take into account the estimated incompleteness of Indigenous identification in each jurisdiction. It is likely that the true death rates for Indigenous people will be closer to these rates than to those based solely on death registrations.

4 Note figures have not been adjusted for reporting delay. The figures quoted here are aggregated nationally, and may conceal differences across Australia, particularly between rural/remote and urban areas, for which the patterns may be quite different.

5 Defined as less than the third percentile of World Health Organization reference values.

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Last updated: 26 July 2005