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Introduction | Methods | Results - Part 1 | Acknowledgements | Appendices | References
Results: Bloodborne diseases | Gastrointestinal | Quarantinable | Sexually transmissible | Vaccine preventable | Vectorborne | Zoonoses | Other bacterial infections
Results - Part 3
Sexually transmissible infections
Introduction
In 2011, the sexually transmissible infections (STIs) reported to the NNDSS were chlamydial infection, donovanosis, gonococcal infection and syphilis. Other national surveillance systems that monitor STIs in Australia include the Australian Gonococcal Surveillance Programme (AGSP), which is a network of specialist laboratories monitoring antimicrobial susceptibility patterns of gonococcal infection; and the Kirby Institute, which maintains the National HIV Registry and the National AIDS Registry.
In interpreting these data it is important to note that changes in notifications over time may not solely reflect changes in disease prevalence as changes in screening programs,25,26 the use of less invasive and more sensitive diagnostic tests and periodic public awareness campaigns may influence the number of notifications that occur over time. Rates for STIs, are particularly susceptible to overall rates of testing, with low testing rates resulting in an underestimation of disease and increased testing potentially causing an increase in notifications.27 For some diseases, changes in surveillance practices may also need to be taken into account when interpreting national trends.
It is important to note that data is reported by diagnosis date, a derived field, with the exception of syphilis in Queensland which is reported by notification receive date. These data may not be directly comparable with data in state and territory communicable disease reports, which report by onset date or notification date, but the trends that they highlight should be comparable.
Direct age standardised notification rates, using the method described by the Australian Institute of Health and Welfare28 were calculated for Aboriginal and Torres Strait Islander and non-Indigenous notifications for jurisdictions that had Indigenous status data completed for more than 50% of notifications over the period 2006–2011. Where the Indigenous status of a case was not completed, these notifications were counted as non-Indigenous in the analyses. These data, however, should be interpreted with caution, as STI screening occurs predominately in specific high risk groups, including in Aboriginal and Torres Strait Islander populations. The differences in rates between females and males should be interpreted with caution, as rates of testing for STIs, symptom status, health care-seeking behaviours, and partner notification differ between the sexes.29
In the national case definitions for chlamydial, gonococcal and syphilis infections the mode of transmission cannot be inferred from the site of infection. Infections in children may be acquired perinatally (e.g. gonococcal conjunctivitis).30 Notifications of chlamydial, gonococcal and non-congenital syphilis infections were excluded from analysis where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Chlamydial infection
Genital chlamydia infection is caused by the bacterium Chlamydia trachomatis serogroups D–K. The infection is asymptomatic in approximately 1%–25% of sexually active men and up to 70% of sexually active women.14 Men with asymptomatic infection act as carriers transmitting the infection while only rarely suffering from long term health problems. However, in women there is a high risk of developing severe health conditions as a result of the infection, including infertility and pelvic inflammatory disease.14,31
Epidemiological situation in 2011
Chlamydial infection continued to be the most commonly notified disease in 2011. Since chlamydial infection became a nationally notifiable disease in 1991 (1997 in New South Wales), the rate has increased in each consecutive year. In 2011, there were 80,800 notifications of chlamydial infection, equating to a rate of 357.2 per 100,000. This represents an increase of 7.2% compared with the rate reported in 2010 (333.1 per 100,000). Between 2006 and 2011, chlamydial infection rates increased by 56%, from 229.1 to 357.2 per 100,000.
Geographical distribution
Increasing rates of chlamydia were reported from all states and territories with the Northern Territory (1,141.6 per 100,000), Western Australia (496.9 per 100,000) and Queensland (407.2 per 100,000) substantially higher than the national rate (Table 4).
Age and sex distribution
In 2011, rates of chlamydial infection in males and females were 296 and 416 per 100,000 respectively. When compared with 2010, rates increased by 6% in males and 8% in females. Rates in females exceeded those in males prior to the age of 30 years, especially in the 10–14 year age group with a male to female ratio of 0.1:1, while males have higher rates in older age groups (Figure 17). The overall rate in females exceeded those in males with a ratio of 0.7:1, which may be partly attributable to preferential testing of women attending health services compared with men.10,32
Figure 17: Notification rate for chlamydial infection, Australia, 2011, by age group and sex*
* Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 17 (TXT 1 KB)
Between 2006 and 2011, there was an increasing trend in chlamydia notification rates across both sexes and in all age groups (Figure 18). The greatest increase in rates amongst those aged between 15 and 39 years occurred in both males and females in the 15–19 (100% and 76% respectively) age group. Those between 15 and 29 years of age accounted for approximately 80% of the annual number of reported cases during the period 2006–2011.
Figure 18: Notification rate for chlamydial infection in persons aged 10–39 years, Australia, 2006 to 2011, by age group and sex*
* Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 18 (TXT 1 KB)
Indigenous populations
Data on Indigenous status were complete in 51% of notifications in 2011, higher than the preceding 5-year average of 47% (range: 44%–51%). It should be noted that the completeness of Indigenous status identification in the notification data varies by year and by jurisdiction. Four jurisdictions had greater than 50% completeness of the Indigenous status field across the 2006 to 2011 period: the Northern Territory, South Australia, Tasmania and Western Australia. Amongst these jurisdictions, the combined age standardised notification rate ratio between Aboriginal and Torres Strait Islander and non-Indigenous populations in 2011 was 3.5:1.
Rates amongst the Aboriginal and Torres Strait Islander population remained fairly consistent between 2006 and 2009, with an average rate during this period of 1,205 per 100,000. Between 2010 and 2011 there was a 21% increase to 1,366 per 100,000. Rates amongst the non-Indigenous population have been trending upwards from a rate of 235 per 100,000 in 2006 to 393 per 100,000 in 2011, a 67% increase over this period.
In 2011 chlamydia rates increased compared with 2010 in all 4 states and territories in which Indigenous status was more than 50% complete, the proportion of cases that were of Aboriginal or Torres Strait Islander origin ranged from 1% in Western Australia to 17% in Tasmania. Amongst the non-Indigenous population chlamydia rates decreased in Tasmania (11%) and the Northern Territory (7%) and increased in South Australia (18%) and Western Australia (14%) (Figure 19). The overall high Aboriginal and Torres Strait Islander rates observed in the Northern Territory may be partly explainable by the high levels of screening that take place in remote Aboriginal and Torres Strait Islander communities.
Figure 19: Age standardised rates for chlamydial infection, selected states and territories,* 2006 to 2011, by Indigenous status
* Includes notifications in the Northern Territory, South Australia, Tasmania and Western Australia where Indigenous status was reported for more than 50% of cases between 2006 and 2011.
Text version of Figure 19 (TXT 1 KB)
Donovanosis
Donovanosis, caused by the bacterium Klebsiella granulomatis, is a chronic, progressively destructive infection that affects the skin and mucous membranes of the external genitalia, inguinal and anal regions.33 Donovanosis was targeted for elimination in Australia through the National Donovanosis Elimination Project, which commenced in 2001.34 It predominantly occurred in rural and remote Aboriginal and Torres Strait Islander communities in central and northern Australia and is now relatively uncommon.
Epidemiological situation in 2011
There were no notifications of donovanosis in 2011 (Figure 20).
Figure 20: Notifications of donovanosis, Australia, 1991 to 2011, by sex
Text version of Figure 20 (TXT 1 KB)
Gonococcal infections
Gonorrhoea is caused by the bacterium Neisseria gonorrhoeae which affects the mucous membranes causing symptomatic and asymptomatic genital and extragenital tract infections.14
Epidemiological situation in 2011
In 2011, there were 12,087 notifications of gonococcal infection, a rate of 53 per 100,000. This was an 18.9% increase compared with 2010.
Geographical distribution
The highest rate in 2011 was in the Northern Territory (849 per 100,000), which was approximately 16 times higher than the national rate (Table 5). All states and territories except Tasmania and South Australia reported increases in rates ranging from 1% in the Northern Territory to 124% in the Australian Capital Territory compared with 2010.
Age and sex distribution
Nationally, there was an increase in gonococcal infection rates in both males (18%) and females (27%) compared with 2010. The male to female rate ratio in 2011 was 2.0:1 (72 and 35 per 100,000 respectively), which is similar to the previous 5 years. The rate of gonococcal infection in males exceeded those in females in all age groups except those less than 20 years of age (Figure 21).
Figure 21: Notification rate for gonococcal infections, Australia, 2011, by age group and sex*
* Excludes notifications for whom age or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 21 (TXT 1 KB)
Age specific rates amongst males and females increased in all age groups with a marked increase amongst the 15–19 year age group reported for males and females. (Figure 22).
Figure 22: Notification rate for gonococcal infection in persons aged 10–49 years, Australia, 2006 to 2011, by age group and sex*
* Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 22 (TXT 1 KB)
Indigenous populations
In 2011, the data completeness of the Indigenous status field for gonococcal infection notifications was 68%, slightly higher than 2010 (65%) but a decrease compared with the previous few years (average completeness 69%). All jurisdictions except New South Wales and the Australian Capital Territory had greater than 50% completeness of the Indigenous status field. Amongst these jurisdictions with adequate completeness, the combined age standardised notification rate for gonococcal infection in the Aboriginal and Torres Strait Islander population had been steadily declining from 923 per 100,000 in 2006 to 642 per 100,000 in 2009 before increasing to 746 per 100,000 in 2010 and 894 per 100,000 in 2011. In the non-Indigenous population, rates remained stable at around 22 to 23 per 100,000 between 2006 and 2009 before also increasing by 35% to 31 per 100,000 in 2011. Between 2006 and 2011 the Aboriginal and Torres Strait Islander to non-Indigenous rate ratio decreased 30% from 41:1 to 28:1. In 2011, rates of gonococcal infection in the Aboriginal and Torres Strait Islander and non-Indigenous populations decreased or remained relatively stable compared with 2010 in all jurisdictions except Queensland and Western Australia (Figure 23).
Figure 23: Age standardised rates for gonococcal infection, selected states and territories,* 2006 to 2011, by Indigenous status
* Includes notifications in the Northern Territory, Queensland, South Australia, Tasmania, Victoria and Western Australia where Indigenous status was reported for more than 50% of cases over a 5-year period.
Text version of Figure 23 (TXT 1 KB)
The overall high Aboriginal and Torres Strait Islander rates observed in the Northern Territory may be partly explained by the high levels of screening that take place in remote Aboriginal and Torres Strait Islander communities.
Microbiological trends
The AGSP is the national surveillance system for monitoring the antimicrobial resistance of N. gonorrhoeae isolates, via a network of public and private reference laboratories located in each jurisdiction. Susceptibility testing, using a standardised methodology, is performed on gonococcal isolates to a core group of antibiotics: penicillin, ceftriaxone, spectinomycin, quinolone and tetracycline.
In 2011, the AGSP annual report for 201135 reported a total of 4,230 gonococcal isolates were tested for antibiotic susceptibility, representing approximately 35% of gonococcal infection notifications, which was a slightly lower proportion to 2010 (41%) and 2009 (40%).
Of the isolates collected through the AGSP in 2011, the majority (3,403) were from males with the remaining 827 being from females (ratio 4:1). In males, 68% of isolates were obtained from the urethra, 18% from the rectum and 12% from the pharynx. In females, the majority of isolates (86%) were obtained from the cervix.
In 2011, approximately 25% of gonococcal isolates had some level of resistance to the penicillins, a decrease from the 29% in 2010. In addition, 27% had some level of resistance to quinolones, a further decrease in proportion of quinolone resistance from 35% in 2010 and 43% detected in 2009. Since 2001, low but increasing numbers of isolates with decreased susceptibility to ceftriaxone have been identified in Australia with 3.2% observed nationally in 2011. For more details see the AGSP annual report series published in CDI.
Discussion
From 2006 to 2011 there was an increase in the notification rate of gonorrhoea. Preliminary findings from analysis of notification data from 2007 to 2011 indicated that there is no evidence to suggest the overall increase in notifications was due to an increase in a particular sub-group (e.g. Indigenous populations). These analyses also suggest there may be 2 separate epidemics occurring in men who have sex with men in eastern states and amongst women in more remote areas with greater Indigenous populations (unpublished analysis).
Syphilis (non-congenital categories)
Syphilis, caused by the bacterium Treponema palladium, is characterised by a primary lesion, a secondary eruption involving skin and mucous membrane, long periods of latency and late lesions of skin, bone, viscera, cardiovascular and nervous systems.14
In 2004, all jurisdictions except South Australia began reporting to the NNDSS of non-congenital syphilis infections categorised as: infectious syphilis (primary, secondary or early latent) of less than 2 years duration; and syphilis of more than 2 years or unknown duration. South Australia, only report cases of infectious syphilis. Detailed analyses are reported for these 2 categories, as well as for syphilis of the combined categories (syphilis – all categories) for the purpose of showing trends in previous years. Data for all states and territories are reported by diagnosis date, except Queensland, which is reported by notification receive date. During this reporting period, the syphilis case definition was applied differently in Queensland compared with the rest of Australia. The aggregated data are presented with this variation in place.
Epidemiological situation in 2011
In 2011, there were 2,563 notifications of syphilis in all non-congenital categories, representing a rate of 11.3 per 100,000, a 4.6% increase compared with 2010 (10.8 per 100,000) (Table 5, Figure 24).
Figure 24: Notification rate for non-congenital syphilis infection (all categories), Australia, 2006 to 2011
* Excludes notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 24 (TXT 1 KB)
Geographical distribution
The Northern Territory continued to have the highest rate of syphilis (38.6 per 100,000), however this was a marked decline compared with 2010 (61 per 100,000). New South Wales was the only other state to report a decrease in rates. The remaining states and territories reported an increase in rates ranging from 3% in Victoria to 94% in South Australia.
Syphilis – infectious (primary, secondary and early latent), less than 2 years duration
Epidemiological situation in 2011
In 2011, there were 1,303 notifications of infectious syphilis (primary, secondary and early latent), of less than 2 years duration. This represents a notification rate of 5.8 per 100,000, an increase of 13.7% compared with 2010 (5.1 per 100,000) (Table 5). The rate of infectious syphilis notifications increased from 4.3 per 100,000 in 2006 to a peak of 6.8 per 100,000 in 2007 and gradually declined until 2010 with an increase in 2011. The Northern Territory had the highest notification rate at 13.0 per 100,000 in 2011, a 31% decrease compared with 2010.
Age and sex distribution
Rates of infectious syphilis for males and females were 10.0 and 1.5 per 100,000 respectively, representing a male to female ratio of 7:1 (Table 12). Rates in males were highest in the 40–44 year age group (22.5 per 100,000), followed by the 30–34 and 35–39 year age groups (19.5 and 19.1 per 100,000 respectively), whereas in females the highest notification rates were observed in the 15–19 year age group followed by the 20–24 and 25–29 year age groups (5.9, 4.7 and 2.9 per 100,000 respectively) (Figure 25).
| Male | Female | Total‡ | ||||
|---|---|---|---|---|---|---|
| State or territory | Count | Rate† | Count | Rate† | Count | Rate† |
| * Excludes notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired. † Notification rate per 100,000 population. ‡ Includes notifications that have missing sex. | ||||||
ACT/NSW |
416 |
10.9 |
14 |
0.4 |
431 |
5.6 |
NT |
14 |
11.7 |
16 |
14.4 |
30 |
13.0 |
Qld |
262 |
11.4 |
70 |
3.1 |
332 |
7.2 |
SA |
24 |
3.1 |
12 |
1.4 |
45 |
2.8 |
Tas. |
5 |
2.0 |
1 |
0.4 |
6 |
1.2 |
Vic. |
295 |
10.6 |
31 |
1.1 |
330 |
5.9 |
WA |
105 |
8.8 |
22 |
1.9 |
127 |
5.4 |
Total |
1,121 |
10.0 |
166 |
1.5 |
1,301 |
5.8 |
Figure 25: Notification rate for infectious syphilis (primary, secondary and early latent), less than 2 years duration, Australia, 2011, by age group and sex*
* Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 25 (TXT 1 KB)
From 2006 to 2007 notification rates amongst males increased substantially in the 20–49 year age range. Since 2007, 20–29 and 30–39 year age groups have either decreased or remained relatively stable. The 40–49 year age group experienced a marked increase between 2010 and 2011. In females, for the 2006 to 2011 period, rates remained relatively steady, except in the 15–19 year age group where they decreased from a peak of 7.7 per 100,000 in 2006 to 1.8 per 100,000 in 2010 and then increased to 5.9 per 100,000 in 2011 (Figure 26).
Figure 26: Notification rate for infectious syphilis (primary, secondary and early latent), less than 2 years duration, in persons aged 10 years or over, Australia, 2006 to 2011, by age group and sex*
* Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 26 (TXT 1 KB)
Indigenous populations
In 2011, data on Indigenous status was complete for 94% of infectious syphilis notified cases. All jurisdictions except the Australian Capital Territory had greater than 50% completeness of the Indigenous status field between 2006 and 2011. The age standardised notification rate was 29 per 100,000 in the Aboriginal and Torres Strait Islander population and 5.0 per 100,000 in the non-Indigenous population, representing a rate ratio of 6:1. In 2011, Aboriginal and Torres Strait Islander rates in all states and territories, except New South Wales and the Northern Territory, increased when compared with 2010. The increase evident in Aboriginal and Torres Strait Islander rates in Western Australia in 2008 was largely attributable to an outbreak that occurred in 2008 in the Pilbara region amongst Aboriginal people (Figure 27).36 Nationally, there has been a 28% decrease in Aboriginal and Torres Strait Islander rates (from 40 to 29 per 100,000) between 2006 and 2011.
Figure 27: Age standardised rates for infectious syphilis, selected states and territories,* 2006 to 2011, by Indigenous status
* Includes notifications in the Northern Territory, Queensland, South Australia, Tasmania, Victoria, Western Australia and New South Wales where Indigenous status was reported for more than 50% of cases over a 5-year period.
Text version of Figure 27 (TXT 1 KB)
Syphilis of more than 2 years or unknown duration
Epidemiological situation in 2011
In 2011, there were 1,260 notifications of syphilis of more than 2 years or unknown duration, a rate of 6.0 per 100,000, which is similar to the rate in 2010 (6.1 per 100,000).
Age and sex distribution
In 2011, notification rates of syphilis of more than 2 years or unknown duration in males and females were 7.9 and 4.0 per 100,000, respectively (Table 13), with a male to female rate ratio of 2.0:1 (Figure 28). Age group specific rates in males were higher than in females except in the 10–14 and 15–19 age groups, and were more than 3 times higher amongst males in the 50–54 and 60–64 year age groups than in females. The distribution of notification rates across age groups in females was bimodal, with the highest rate (7.9 per 100,000) amongst those in the 80–84 year age group, followed by those in the 35–39 year age group (7.5 per 100,000). In males, rates remained high in those aged 25 years or over with peaks occurring in the 40–44 year and 85 years or over age groups (13.9 and 20.3 per 100,000 respectively).
Figure 28: Notification rate for syphilis of more than 2 years or unknown duration, Australia,* 2011, by age group and sex†
* Data from all states and territories except South Australia.
† Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 28 (TXT 1 KB)
| Male | Female | Total§ | ||||
|---|---|---|---|---|---|---|
| State or territory | n | Rate | n | Rate | n | Rate |
| * Excludes notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired. † Notification rate per 100,000 population. ‡ Data from all states and territories except South Australia. § Includes notifications missing sex. NDP- No data provided. | ||||||
ACT/NSW |
220 |
5.8 |
112 |
1.5 |
332 |
4.3 |
NT |
41 |
34.4 |
18 |
7.8 |
59 |
25.6 |
Qld |
132 |
5.8 |
87 |
1.9 |
221 |
4.8 |
SA |
NDP |
– |
NDP |
– |
NDP |
– |
Tas. |
12 |
4.8 |
8 |
1.6 |
20 |
3.9 |
Vic. |
365 |
13.1 |
158 |
2.8 |
530 |
9.4 |
WA |
58 |
4.9 |
38 |
1.6 |
96 |
4.1 |
Total |
829 |
7.9 |
421 |
4.0 |
1,258 |
6.0 |
Over the period 2006 to 2011, rates amongst most age groups in males have decreased with a substantial decrease of 42% observed amongst males in the 15–19 year age group. Over the same period, rates in females have decreased in all age groups with the largest declines reported amongst the 15–19 and 20–29 year age groups (56% and 37% respectively) (Figure 29).
Figure 29: Notification rate for syphilis of more than 2 years or unknown duration, Australia,* 2006 to 2011, by age group and sex†
* Data from all states and territories except South Australia.
† Excludes notifications for whom age and/or sex were not reported and notifications where the case was aged less than 13 years and the infection was able to be determined as non-sexually acquired.
Text version of Figure 29 (TXT 1 KB)
Congenital syphilis
Epidemiological situation in 2011
Following a peak of 19 notifications in 2001, notifications of congenital syphilis have continued to decline (Figure 30). Antenatal screening for congenital syphilis is considered to be a contributor to this decline.37 There were 6 notifications of congenital syphilis in 2011; 2 females and 1 male from Queensland and 2 males and 1 female from New South Wales. Three of the cases were reported as Aboriginal and Torres Strait Islander and three were non-Indigenous.
Figure 30: Trends in notifications of congenital syphilis, Australia, 1999 to 2011
Text version of Figure 3 (TXT 1 KB)
Vaccine preventable diseases
Introduction
This section summarises the national surveillance data for notifiable diseases targeted by the National Immunisation Program (NIP) in 2011. These include diphtheria, invasive Haemophilus influenzae type b infection, laboratory-confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease, poliomyelitis, rubella, tetanus and varicella zoster infections (chickenpox, shingles and unspecified). Data on hepatitis B and invasive meningococcal disease, which are also targeted by the NIP, can be found in this report under ‘Bloodborne diseases’ and ‘Other bacterial infections’ respectively. Other vaccine preventable diseases (VPDs) presented in this report include hepatitis A and Q fever under the ‘Gastrointestinal’ and ‘Zoonoses’ sections respectively. For more detailed reports on historical data, including notifications, hospitalisations and deaths, readers are referred to the regular CDI supplements ‘Vaccine Preventable Diseases in Australia’, the latest of which was published as the December 2010 supplement issue of CDI.38 Additionally, a similar report which analyses the impacts of vaccines on the health of Aboriginal and Torres Strait Islander people between 2007 and 2010 was published in the November 2013 supplement to CDI.39
In 2011, there were 81,872 VPD cases reported to the NNDSS, representing 34% of all reported cases and a 32% increase compared with 2010 (62,009 cases). Pertussis was the most commonly notified VPD with 38,602 cases (47%) reported, reflecting the continued high levels of pertussis activity in 2011; followed by influenza (27,149, 33%). The number of notifications and notification rates for VPDs in Australia are shown in Tables 3 and 4.
New vaccines added to the National Immunisation Program in 2011
In 2011, a pneumococcal conjugate 13-valent (13vPCV) vaccine for infants aged 2, 4 and 6 months and medically at-risk children was introduced onto the NIP. A single catch-up dose was also funded from 1 October 2011 until 30 September 2012 for children aged between 12 months and 35 months who had already completed a primary pneumococcal vaccination.
Vaccination coverage is an important factor influencing the incidence of vaccine preventable diseases. Since the commencement of the Australian Childhood Immunisation Register in 1996, immunisation coverage in Australian children has been high by international standards, although geographical pockets of lower coverage remain, in which there is an increased potential for VPDs to occur and circulate. No vaccine is 100% effective, and therefore infections sometimes do occur in fully vaccinated people, and some are reported later in this section. However, effective vaccines do provide a substantially lower chance of becoming infected, and/or reduced the severity of the disease.
Information on the receipt of vaccines has historically been recorded in NNDSS using the ‘vaccination status’ field (fully or partially vaccinated for age or unvaccinated), plus a field capturing the number of doses. In January 2008 new, more detailed fields were added for recording ‘vaccine type’ and ‘vaccination date’ for each dose. The new fields were intended to replace the old fields, with a transition period allowing either field to be utilised. In 2011, 4 jurisdictions were using the new fields (the Northern Territory, Queensland, Tasmania and New South Wales for selected diseases), while the remaining jurisdictions continued to use the old fields. In this report, data on receipt of vaccines is presented for each disease, combining data provided by the states and territories from the two different formats.
Diphtheria
Diphtheria is an acute toxin-mediated systemic disease caused by the bacterium Corynebacterium diphtheriae. Infection is usually localised to the throat (pharyngeal diphtheria) in which a membranous inflammation of the upper respiratory tract can cause airway obstruction, or the skin (cutaneous diphtheria). Systemic complications caused by the bacterium’s exotoxin can occur in both pharyngeal and cutaneous diphtheria. Diphtheria is spread by respiratory droplets or by direct contact with skin lesions or articles soiled by infected individuals.16 While there are non-toxigenic strains of C. diphtheriae, they usually only cause mild throat or skin infection and are not nationally notifiable.
Epidemiological situation in 2011
There were 4 notifications of diphtheria in 2011. A cluster of 3 pharyngeal cases were diagnosed in Queensland and 1 unrelated case of cutaneous diphtheria was acquired in Indonesia and diagnosed in the Northern Territory. The index case in the Queensland cluster had recently returned from Papua New Guinea, where it is likely that they acquired their infection. This case was confirmed as being a pharyngeal carrier of penicillin resistant Corynebacterium diphtheriae. The second case in this cluster, who subsequently died, was a close contact of the index case and the third was an asymptomatic case who was identified through contact tracing. Queensland Health followed up close contacts of the cases and provided prophylactic treatment where required as per their public health guidelines.
Age and sex distribution
The male to female ratio was 1:1 comprising 2 cases each. Three cases, including the fatal case, were in the 20–24 year age group and the fourth was over 85 years of age.
Vaccination status
Two of the 3 cases in the Queensland cluster were vaccinated including the index case and the asymptomatic contact, while the third case, who died, was unvaccinated. The case of cutaneous diphtheria was also vaccinated.
Discussion
In the decade between 1926 and 1935 over 4,000 deaths from diphtheria were reported.38 A vaccine for diphtheria was introduced in Australia in 1932 and since then both cases and deaths have virtually disappeared. Prior to the cases reported in 2011, the last Australian case was one of cutaneous diphtheria in 2001 acquired in East Timor and the last deaths, of which there were two, occurred between 1986 and 1995. In Australia, serosurveillance data indicate that childhood immunity to diphtheria is greater than 99%. However, waning immunity amongst adults may result in this population being susceptible, with the most likely source of exposure being through overseas travel to countries where diphtheria remains endemic.40 The 2011 Queensland cluster highlights the importance of maintaining high vaccination coverage to protect against vaccine preventable diseases that remain endemic in many other countries around the world.
Influenza
Epidemiological situation in 2011
Notifications of influenza increased substantially compared with previous years, with the exception of the 2009 pandemic year. There were 27,149 notifications of laboratory-confirmed influenza in 2011, more than twice the number of cases from the previous year (n=13,419).
Notification rates were highest in South Australia (286 per 100,000), followed by the Northern Territory (259 per 100,000) and Queensland (227 per 100,000). Notification rates in the remaining jurisdictions were all substantially lower than the national notification rate of 120 per 100,000. In 2011, Queensland reported a larger number of influenza cases than any other jurisdiction, comprising 38% of all notifications, which was consistent with previous years with the exception of 2010 (Figure 31).
Figure 31: Notifications of laboratory-confirmed influenza, Australia, 2011, by week and state or territory
Text version of Figure 31 (TXT 1 KB)
Age and sex distribution
Females accounted for 14,323 (53%) of the 27,119 influenza notifications for which sex was reported in 2011. Notifications rates were higher amongst females in most age groups, with the primary exception of those aged less than 15 years where the rates were higher for males (Figure 32). This likely reflects the health seeking behaviour of adult females as they tend to account for a greater proportion of encounters in general practice.41
Figure 32: Notifications of laboratory-confirmed influenza, Australia, 2011, by age group and sex*
* Excludes 44 notifications for which age and/or sex were not reported.
Text version of Figure 32 (TXT 1 KB)
The highest number of influenza notifications occurred in the 0–4 year age group and accounted for 14% of all notifications. Similarly, notification rates were highest in the 0–4 and 5–9 year age groups (255 and 227 notifications per 100,000, respectively) (Figure 33). More than half of all influenza notifications were in persons aged less than 30 years.
Figure 33: Notification rate for laboratory-confirmed influenza, Australia, 2006 to 2011, by age group and year
Text version of Figure 33 (TXT 1 KB)
Seasonality
Higher than usual numbers of influenza notifications during the 2010–11 inter-seasonal period were reported in all jurisdictions, especially in Queensland and the Northern Territory. The 2011 season peaked in August with 7,690 cases for the month, compared with the lower peak of 4,981 notifications during September 2010 (Figure 34). Notifications fell substantially through October and returned to typical inter-seasonal levels by late November 2011.
Figure 34: Notifications of laboratory-confirmed influenza, Australia, 2007 to 2011, by month and year
Text version of Figure 34 (TXT 1 KB)
Virological surveillance
In 2011, almost all (>99%, n=27,049) of the influenza notifications in NNDSS had some level of influenza typing reported. Of those with type information, 73% were type A (40% A (unsubtyped), 26% A(H1N1)pdm09, 7% were A(H3N2)) and almost 27% were type B. Mixed influenza type A and B infections, and influenza type C together accounted for less than 1% of notifications (Figure 35). In comparison, in 2010 the proportion of notifications reported as influenza type A was much higher (90%), with the majority of these (56%) reported as A(H1N1)pdm09, followed by A(unsubtyped) (30%), with very few A(H3N2) (4%). Additionally, the proportion of influenza B notifications in 2010 was substantially less (10%) than in 2011. Mixed influenza type A and B infections also accounted for less than 1% of notifications and typing data were not available for 18 cases in 2010.
Figure 35: Notifications of laboratory-confirmed influenza,* Australia, 2011, by week and subtype
* Excluding mixed type A and B, type C and untyped influenza infections.
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The WHO Collaborating Centre for Reference and Research on Influenza (WHOCC) typed and subtyped 2,377 influenza virus samples that were collected in 2011. This represented 8.8% of the 27,149 laboratory confirmed cases reported to the NNDSS. Influenza A(H1N1)pdm09 comprised 46% of influenza viruses, followed by influenza B (29%; consisting of 98.3% B/Victoria lineage and 1.7% B/Yamagata lineage viruses) and influenza A(H3N2) (24%).
All 3 strains of the 2011 Southern Hemisphere influenza vaccine were the same as those previously recommended in the 2010 Southern Hemisphere vaccine. The 2011 Australian influenza vaccine contained an A/California/7/2009 (H1N1)-like virus, an A/Perth/16/2009 (H3N2)-like virus and a B/Brisbane/60/2008-like virus. The WHOCC conducted antigenic characterisation by haemagglutination inhibition assays on 2,177 influenza virus isolates. The majority (79%) of A(H1N1)pdm09 isolates were characterised as A/California/7/2009-like, while the remainder were characterised as ‘low reactor’ compared with the reference virus. Of the circulating influenza A(H3N2) viruses analysed, nearly all (98%) were antigenically similar to the A/Perth/16/2009 virus. Similarly, most (89%) influenza B viruses detected were closely related to the B/Brisbane/60/2008 virus (a B/Victoria lineage virus). A small number (n=7) of influenza B viruses were closely related to the B/Florida/4/2006 virus (B/Yamagata lineage). Thus, the majority of circulating viruses that were isolated in 2011 were antigenically similar to the 2011 vaccine viruses.
Viruses collected in 2011 were also tested for antiviral susceptibility and resistance to the neuraminidase inhibitor class of antiviral drugs (oseltamivir and zanamivir). Neuraminidase inhibition (NAI) assay was performed on 2,173 viral isolates. Twenty-four of the A(H1N1)pdm09 isolates tested showed resistance to oseltamivir and two showed resistance to zanamivir. Pyrosequencing of 157 A(H1N1)pdm09 clinical specimens (these samples were influenza positive but virus was not able to be isolated from them for the NAI assay) found 15 specimens with the H275Y mutation, which is known to confer oseltamivir resistance. Therefore a total of 39 (3.6%) A(H1N1)pdm09 viruses showed oseltamivir resistance. No oseltamivir or zanamivir resistance was detected in any of the A(H3) or influenza B viruses.
Discussion
Higher than usual levels of influenza activity characterised the 2010–11 inter-seasonal period and contributed to the increase in notifications, compared with the previous year. There were 4,207 notifications in the first 5 months of 2011, compared with just 934 in the same period of 2010. Most of the influenza activity during this period was attributed to A(H1N1)pdm09 and A(H3N2) infections. The reason for the unusually high activity is not clear but does not appear to be solely due to increased testing. It is worth noting that the 2010–11 inter-seasonal period was characterised by extensive flooding, particularly in Queensland, which may have been associated with increases in influenza A virus survival rates,42 and time spent indoors.
The main 2011 winter season commenced and peaked earlier than the previous year, although the timing of peaks and the distribution of subtypes varied by jurisdiction. While the majority of virus detections were reported as influenza A(unsubtyped), the season was characterised as a A(H1N1)pdm09 season, with co-circulation of influenza B. In comparison to 2010, the proportion of A(H1N1)pdm09 notifications fell from 56% to 26% in 2011. The shift to increasing proportions of influenza A(H3N2) and type B was associated with an increase in notifications rates for people aged 70 years or over. This contrasts with the pandemic dominant year of 2009, which was characterised by decreasing notifications rates by increasing age.
The number of laboratory confirmed notifications of influenza in 2011 was more than twice that of the previous year. Other influenza surveillance systems indicate that the increase in activity through the main winter season is not significant compared with 2010, and may be a result of, at least in part, increased testing, including differential testing rates between jurisdictions.
Invasive Haemophilus influenzae type b disease
Invasive Haemophilus influenzae type b (Hib) bacteria cause disease with symptoms dependant on which part of the body is infected. These include: septicaemia; meningitis; epiglottitis; pneumonia; osteomyelitis and cellulitis.
Epidemiological situation in 2011
There were 13 notifications of Hib disease reported in 2011, a little over half of the 24 reported in 2010 and a ratio of 0.6 compared with the mean notifications during the previous 5 years. The rate in 2011 was 0.1 per 100,000 and consistent with the very low rates since the Hib vaccine was included in NIP in July 1993 (Figure 36). Cases occurred in Queensland (n=5), New South Wales (n=4), the Northern Territory (n=2), and one each in Victoria and Western Australia. Indigenous status was completed for 100% of cases in 2011. Two cases (15%) were reported as Indigenous, both were notified from the Northern Territory.
Figure 36: Notifications and notification rate for invasiveHaemophilus influenzae< type b infection, Australia, 1992 to 2011
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Age and sex distribution
The male to female ratio was 1.6:1 in 2011 with 8 males and 5 females overall. The majority of cases (n=7) were in children less than 5 years of age, 57% of which were in infants aged less than 1 year. Age group specific rates were highest in the 0–4 year age group (Figure 37).
Figure 37: Notification rate for invasive Haemophilus influenzae type b infection, Australia, 2011, by age group and sex
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Vaccination status
Since the introduction of the Hib vaccine in 1993, there has been a marked reduction in notified cases of Hib in Australia (Figure 36), which now has one of the lowest rates of Hib in the world.38
In 2011, all children under the age of 19 years were eligible for Hib vaccination in infancy, as Hib vaccines were introduced to the NIP in April 1993 for all children born after February 1993. Of the 8 eligible cases in 2011, 7 were fully vaccinated for age and of these, four had received all scheduled doses as recommended under the NIP.
Invasive pneumococcal disease
Invasive pneumococcal disease (IPD) is a clinical condition in which Streptococcus pneumoniae is isolated from a normally sterile site such blood, cerebrospinal fluid or pleural fluid. A universal pneumococcal vaccination program with the 7-valent pneumococcal conjugate vaccine (7vPCV) was introduced onto the NIP for young children in 2005. This was an expansion of the use of the 7vPCV for Aboriginal and Torres Strait Islander and medically at-risk children that was included on the NIP in July 2001. The 7vPCV targets S. pneumoniae serotypes 4, 6B, 9V, 14, 18C, 19F and 23F. From 1 July 2011 a higher valency conjugate vaccine replaced the 7vPCV on the NIP; the 13-valent pneumococcal conjugate vaccine (13vPCV) targets an additional 6 serotypes (1, 3, 5, 6A, 7F, 19A). From 1 October 2011 until 30 September 2012 a supplementary dose of the 13vPCV was made available under the NIP to eligible children who had completed their primary pneumococcal vaccination course with the 7vPCV. Vaccination with the 23-valent pneumococcal polysaccharide vaccine (23vPPV) was added to the NIP schedule for Aboriginal and Torres Strait Islander peoples aged 50 years or over in 1999 and non-Indigenous Australians aged 65 years from January 2005.43
Epidemiologic situation in 2011
There were 1,887 notifications of IPD in 2011, representing a rate of 8.3 per 100,000 population.
This was the highest number and rate reported in any 1 year since prior to the introduction of the universal pneumococcal conjugate vaccine program for young children in 2005. The jurisdictional-specific rate of IPD varied from 7.3 per 100,000 in New South Wales to 56.0 per 100,000 in the Northern Territory.
A rise in IPD due to serotype 1 was observed in Central Australia, initially in school-aged Indigenous children in October 2010. The increase continued throughout 2011, spreading throughout the Northern Territory and into Western Australia and Queensland. Nationally, there were 155 cases of IPD due to serotype 1 reported in 2011 and Indigenous Australians accounted for 71% (n=110) of these cases. Excluding these cases reduced the national rate to 7.7 cases per 100,000. Compared with 2010, the overall number of IPD cases increased by 15%. IPD due to serotype 1 accounted for a large proportion (63%), but not all, of this increase.
Each jurisdiction experienced an increase on the number of cases reported in the previous year. The largest increase at the jurisdictional level was in cases resident in the Northern Territory, where the number of cases increased by 126%, from 57 cases in 2010 to 129 cases in 2011. Most of this increase (85%, n=61) can be attributed to a large outbreak of serotype 1 cases. The increase in cases reported in Queensland and Western Australia also exceeded the average national increase. Cases resident in Queensland increased by 26% from 271 cases reported in 2010 to 341 cases reported in 2011. Only 23% of this increase can be attributed to serotype 1 cases. Cases resident in Western Australia increased by 23% from 198 cases reported in 2010 to 243 cases reported in 2011. All of this increase can be attributed to serotype 1 cases, with 56 cases reported in Western Australia in 2011.
Age and sex distribution
The rate of IPD distributed by age in 2011 was bimodal, with the highest rates reported in the elderly and young children (Figure 38). In the elderly, the highest rate was in those aged 85 years or over (35.2 per 100,000) and in children aged less than 5 years the rate was highest in those aged 1 year (32.3 per 100,000).
Figure 38: Notification rate for invasive pneumococcal disease, Australia, 2011, by age group and sex
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In 2011, males accounted for 54% of cases of IPD, resulting in a male to female ratio of 1.2:1. The rate of disease in males exceeded that in females in almost all age groups (Figure 38).
Seasonality
The seasonal trend of IPD in 2011 followed the trend seen in previous years and that of other respiratory diseases (Figure 39). The number of cases was greatest in the winter months, reaching a peak for 2011 in August (n=257). The seasonal trend was more evident in the distribution of cases aged 5 years or over compared with younger children.
Figure 39: Notifications of invasive pneumococcal disease, Australia, 2011, by month of diagnosis
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Indigenous status
Completeness of Indigenous status reporting in 2011 was high, with 94% (n=1778) of cases reported with a known Indigenous status. Indigenous people made up 17% (n=307) of all notifications. In 2011, the rate of IPD in Indigenous people (53.3 per 100,000) was 8 times the rate of non-Indigenous people (6.7 per 100,000). This is the largest gap in IPD rates since national surveillance commenced in 2002.
The rate of disease in Indigenous people has steadily increased since 2008 (Figure 40). However, the rate of disease in non-Indigenous people, particularly in the 0–4 years age group, has continued the large decrease observed as a result of the introduction of the universal 7vPCV immunisation program in 2005.
Figure 40: Notification rate for invasive pneumococcal disease, Australia, 2002 to 2011, by Indigenous status and age group
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Serotype
An identified serotype was reported in 93% (n=1746) of notified cases of IPD in 2011. In children aged less than 5 there has been a dramatic reduction in disease due to serotypes targeted by the 7vPCV in both the Indigenous and non-Indigenous populations, with this reduction being maintained in 2011 (Figure 41). As few as 5% (n=12) of notifications in children aged less than 5 with a serotype identified were caused by those targeted by the 7vPCV in 2011. In this same age group there was an increase in disease due to the 6 additional serotypes targeted by the 13vPCV, with 63% (n=181) of notifications in 2011 due to one of these 6 serotypes. In Indigenous children, this was largely (67%) due to serotype 1, while in non-Indigenous children serotype 19A was the most common serotype reported (77%).
Figure 41: Notification rate for invasive pneumococcal disease in children aged less than 5 years, Australia, 2002 to 2011, by Indigenous status and serotype group
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Discussion
In 2011, IPD reached its highest level since the introduction of the universal pneumococcal conjugate vaccine program in 2005, with much of this increase attributable to an outbreak of IPD due to serotype 1, which began in Central Australia in late 2010. Despite this, a significant reduction in disease due to serotypes targeted in the 7vPCV in both Indigenous and non-Indigenous populations is clearly demonstrated in the notification data. It is important to note that for the Indigenous population national pre-vaccination data are not available as the program was introduced prior to national surveillance commencement in 2002.
The recent increase in disease due to serotypes 1 and 19a indicates potential for the introduction of the 13vPCV to have a significant impact on IPD in Australia. On-going surveillance will be critical to measuring the impact of this and future vaccine programs and detecting the emergence of non-vaccine serotypes.
More detailed analyses can be found in the IPD annual report series published in CDI.
Measles
Measles is a highly infectious, acute viral illness spread by respiratory secretions, including air-borne transmission via aerosolised droplets. The prodrome, lasting 2–4 days, is characterised by fever and malaise followed by a cough, coryza and conjunctivitis. It is usually followed by a maculopapular rash, which typically begins on the face, and then becomes generalised. Measles can be a severe disease, with complications such as otitis media, pneumonia, and acute encephalitis. Subacute sclerosing panencephalitis is a late, rare (approximately 1 in 100,000 cases) complication of measles, which is always fatal.44
Epidemiological situation in 2011
There were 193 notifications of measles in 2011 representing a rate of 0.9 per 100,000 and 2.6 times the mean notification rate of the previous 5 years. This was the highest number of cases since 1999 when 239 cases were reported (Figure 42).
Figure 42: Notifications and notification rate for measles, Australia, 1997 to 2011
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Increases occurred in all states and territories, except Tasmania where no cases were reported. The majority of cases, and largest increases compared with 2010, occurred in New South Wales (n=90), Victoria (n=39) and the Australian Capital Territory (n=21) (Figure 43).
Figure 43: Notifications of measles, Australia, 2006 to 2011, by state and territory and month of diagnosis
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Indigenous status was known for 95% of cases in 2011 (n=183), and of these, 5.5% (n=10) were reported as Indigenous. These 10 cases were all reported from New South Wales where they represented a significantly higher notification rate compared with non-Indigenous people in that state.45 In temperate climates where measles transmission remains endemic, the majority of cases occur in late winter or early spring. This seasonal pattern is no longer evident in Australia.
Age and sex distribution
The overall male to female ratio was 1:1 in 2011; however, variation in sex distribution occurred across age groups (Figure 44).
Figure 44: Notification rate for measles, Australia, 2011, by age group and sex
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In 2011, age at diagnosis ranged from 0 to 66 years with a median age of 19 years. Rates increased across all age groups in 2011 compared with 2010 (Figure 45). The highest age specific rates occurred in the less than 1 year age group at 3.7 per 100,000. There were 11 cases reported in this group. High rates also occurred in the 10–19 year age group (2.1 per 100,000), reflecting the large number of cases reported in this age group (n=61).
Measles rates remained below 2.5 per 100,000 in all age groups between 2006 and 2011 with the exception of infants aged less than 1 year in 2011 (Figure 45). The fluctuating nature of these rates can be attributed to a general trend of sporadic imported cases that occasionally result in outbreaks of locally acquired infection amongst susceptible contacts.
Figure 45: Notification rate for measles, Australia, 2006 to 2011, by age group
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Vaccination status
Two doses of the measles–mumps-rubella (MMR) vaccine are funded under the NIP for children at 12 months and 4 years of age. The MMR vaccine induces long-term measles immunity in 95% of recipients after a single dose and 99% of recipients after the second dose.44
Of the 193 cases notified in 2011, 172 (89%) were born after 31 December 1969 and eligible for a publicly funded measles-containing vaccine. Of the 18 cases aged between 1 and 3 years of age who were eligible for 1 dose of a measles-containing vaccine, one was fully vaccinated for age and the remaining 17 were not vaccinated. Of the remaining 154 cases 4 years of age or over and eligible for 2 doses, 81 were not vaccinated, 17 were partially vaccinated, 5 were fully vaccinated and 51 were of unknown vaccination status. The 10–19 year age group accounted for 51% (n=41) of the unvaccinated cases amongst those 4 years of age or over. Twenty-two cases occurred amongst those born between 1978 and 1982 (29–33 years in 2011). This cohort has previously been identified as susceptible to measles infection as during their childhood a second dose of a measles containing vaccine was not yet recommended and they were not targeted as part of the 1998 measles control campaign.46 Of these cases, 6 were at least partially vaccinated for age, 5 were not vaccinated and 11 were of unknown vaccination status. Eleven cases occurred in adults born before 1968, a cohort that is considered to have high levels of natural immunity,47 all of them were either unvaccinated or of unknown vaccination status.
Source of infection and outbreaks
The majority of cases in 2011 were either imported (32%, n=61) or import-related (27%, n=53). The remaining 79 cases (41%) were locally acquired with the original source of infection unknown. Eighty four per cent of all imported cases were either from the South East Asia Region (n=26) or the Western Pacific Region (n=25). There were 9 cases imported from the European Region and one from South East Africa.
There were 33 clusters of two or more epidemiologically linked cases in 2011. In all except two of these, transmission was interrupted quickly resulting in an outbreak size of fewer than 10 cases. There were 2 outbreaks with more than 9 cases, the first of which involved 23 locally-acquired cases in western Sydney for which a definitive source of infection could not be established. The second cluster was associated with an imported case from New Zealand and resulted in 23 cases predominantly amongst students at a high school in Canberra and their contacts in both the Australian Capital Territory and neighbouring New South Wales.
Genotyping was available for 73% (n=24) of the outbreaks accounting for 85% of all outbreak cases. Genotypes D4, D8 and D9 were identified amongst outbreak cases across Australia (Figure 46).
Figure 46: Measles clusters, Australia, 2011, by state or territory, genotype and source of infection
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Discussion
In October 2010, at the Western Pacific Regional Committee meeting the Regional goal of measles elimination was re-affirmed (resolution RC61.R7) and the Regional Director was requested to establish regional measles verification mechanisms. A Regional Verification Commission for Measles Elimination (RVC) was established in December 2011 and Professor David Durrheim from Australia was nominated and accepted as a member of this committee. One of the main terms of reference for the RVC was to establish guidelines and the associated procedures and criteria for verifying elimination of measles at the country and regional level. The WHO proposed definition of measles elimination is the absence of endemic measles transmission in a defined geographical area (e.g. region) for greater than or equal to 12 months in the presence of a well performing surveillance system. Endemic transmission is defined as the existence of continuous transmission of indigenous or imported measles virus that persists for greater than or equal to 12 months in any defined geographical area.48
Evidence suggests that endemic measles has been eliminated from Australia, since at least 2005, but possibly earlier.49 Based on the WHO definitions, Australia has maintained this in the intervening years. Outbreaks of measles continue to occur mostly related to unvaccinated or partially vaccinated travellers who have been infected in countries where endemic measles transmission continues and then returned to Australia whilst infectious. Due to the highly infectious nature of measles, local transmission can then occur if susceptible individuals, including infants too young to be protected through vaccination, come into contact with the traveller during their infectious period.
In 2011, no outbreak persisted for more than 12 months with the longest lasting approximately 43 days. Ongoing evidence of high population immunity was demonstrated by the rapid cessation of the majority of outbreaks with only three involving more than three generations of transmission (i.e. 35 to 44 days between onset of disease in the first and the last case).50 Ninety-five per cent of outbreak cases, in all states except New South Wales, were associated with an index case that was imported from overseas. There was no evidence that a single genotype was continuously circulating for 12 months or more. Of concern in 2011 was that 41% of cases in New South Wales had no link to an imported case able to be established, highlighting that surveillance gaps do occur, either because some cases do not seek medical attention or are not diagnosed with measles when they do.51 This underlines the difficulty in identifying measles in Australia where the incidence is low and the health system is no longer familiar with this disease.
As part of the regional verification process Australia, along with all Western Pacific Region member countries, will be required to provide epidemiological and virological evidence of sustaining measles elimination on a background of high quality surveillance in order for Australia and the region to be certified measles-free.
Mumps
Mumps is an acute viral illness transmitted by the respiratory route in the form of air-borne droplets or by direct contact with saliva of an infected person. The characteristic bilateral, or occasionally unilateral, parotid swelling occurs in 60%–70% of clinical cases. However, a high proportion have non-specific symptoms including fever, headache, malaise, myalgia and anorexia, with approximately one-third of infections being asymptomatic. Mumps is a multi-system infection, with orchitis occurring in 20% to 30% of post-pubertal males.14
Epidemiological situation in 2011
In 2011, there were 155 notifications of mumps, a rate of 0.7 per 100,000 and a 60% increase compared with the 97 cases reported in 2010. The number of cases remains low compared with the peak of 582 cases reported in 2007 (Figure 47). Cases in 2011 were reported from all states and territories except the Northern Territory. Rates were highest in New South Wales (0.9 per 100,000) followed by Queensland and Victoria (0.8 per 100,000).
Figure 47: Notifications of mumps, Australia, 2006 to 2011, by state or territory and month of diagnosis
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Indigenous status was reported for 63% of mumps cases, an increase of 13% compared with 2010, and 2% (2/98 cases) were reported as Indigenous.
Age and sex distribution
In 2011, the overall male to female ratio was 1:1 with some variation in the sex ratio amongst age groups, notably where the numbers were small. The highest rates for males occurred in the 30–34 year age group (1.66 per 100,000) and for females in the 15–19 year age group (1.24 per 100,000). Rates were higher for young adults of both sexes compared with other cohorts and ranged from 0.93 to 1.66 per 100,000 for males between 20 and 39 years of age and 0.96 to 1.24 per 100,000 for females between 15 and 39 years of age (Figure 48).
Figure 48: Notification rate for mumps, Australia, 2011, by age group and sex
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There were cases of mumps notified across most age groups with age at diagnosis ranging from 3 to 80 years and with a median age of 30 years. All age group rates in 2011 were higher than in 2010 except those less than 1 year of age, in which there were no cases. The biggest increase in age group rates occurred amongst young adults between 20 and 39 years of age, although they remained lower compared with the peak amongst this cohort in 2007–2008 (Figure 49).
Figure 49: Notification rate for mumps, Australia, 2006 to 2011, by age group
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Vaccination status
The mumps component of the MMR vaccine has been estimated to be the least effective of the 3 components, providing 62%–88% and 85%–95% protection for the first and second doses respectively.52,53 Reduced effectiveness of the mumps vaccine has been demonstrated over time and this waning immunity may at least partially account for the proportion of vaccinated mumps cases and contribute to mumps outbreaks in older vaccinated populations.53
The mumps vaccine was first funded on the NIP available in Australia in 1981 with people born since then eligible for 2 doses of a mumps-containing vaccine.54 In 2011, there were 75 cases of mumps in individuals born after 31 December 1980. One case was aged between 1 and 3 years and eligible for 1 dose and was fully vaccinated for age. The remaining 74 cases were aged 4 years or over. Of these, 9% (n=7) were fully vaccinated for age, 9% (n=7) were partially vaccinated for age, 15% (n=11) were unvaccinated. As mumps notifications are not routinely followed up by all public health units, a further 66% (n=49) had an unknown vaccination status reported.
Pertussis
Pertussis, commonly known as whooping cough, is a highly infectious disease caused by Bordetella pertussis and is spread by respiratory droplets.
Epidemiological situation in 2011
In 2011, there continued to be a large number of cases of pertussis associated with the Australia-wide epidemic that began in mid-2008 (Figure 50). There were 38,602 notifications of pertussis in 2011. This included 3 deaths, all in infants less than 8 weeks of age who were too young to be protected by vaccination. While pertussis remains endemic in Australia with a cyclical pattern of epidemic activity occurring approximately every 3 to 4 years, this latest epidemic has been much larger and more prolonged then earlier outbreaks (Figure 51).
Figure 50: Notifications of pertussis, Australia, 2006 to 2011, by month of diagnosis
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Figure 51: Notifications and notification rate for pertussis, Australia, 1993 to 2011
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Rates varied considerably by state or territory in 2011 with the Australian Capital Territory (227 per 100,000), Queensland (196 per 100,000) and New South Wales (179 per 100,000) all having rates higher than the national rate (171 per 100,000). While the timing of epidemic activity has varied across states and territories, all except South Australia had increased rates in 2011 compared with 2010 and the Australian Capital Territory, New South Wales, Queensland, Victoria and Western Australia all reported their highest rates since the epidemic began. The largest increase in activity in 2011 occurred in Western Australia, which increased from a rate of 63 per 100,000 in 2010 to 170 per 100,000 in 2011. In contrast, rates in South Australia declined sharply from a peak of 450 per 100,000 in 2010 to 142 per 100,000 in 2011 (Figure 52).
Figure 52: Notification rate for pertussis, 2006 to 2011, by state and territory
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Age and sex distribution
In 2011, females accounted for 56% (n=21,512) of cases, resulting in a male to female ratio of 0.8:1. Forty-one cases had no sex specified and an additional 20 had no age provided. Females had higher rates across all age groups except for those adults 80 years of age or over (Figure 53). The highest rate in both males and females occurred in the 5–9 year age group (530 and 573 per 100,000 respectively). The largest difference in sex distribution occurred in the 25–29, 30–34 and 35–39 year age groups where rates in females were 2 times that of males, likely representing the increased health seeking behaviour noted in adult females compared with males.41
Figure 53: Notification rate for pertussis, Australia, 2011, by age group and sex
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Rates in 2011 varied widely with age. Children less than 15 years of age had a higher rate (422 per 100,000) than those adolescents and adults 15 years of age or over (112 per 100,000) representing a rate ratio of 3.8:1. This is consistent with the trend of increasing rates amongst children during this epidemic period but differs with the pre-epidemic years in which adults had a higher rate relative to children (rate ratios of 0.7:1, 0.3;1 and 0.5:1 respectively for 2005, 2006 and 2007).
Between 2006 and 2007, a period inclusive of the last national epidemic in 2005–2006, rates in all age groups were either trending down or remaining relatively constant and were closely clustered. Since 2007, rates have been increasing and most markedly amongst those less than 15 years of age (Figure 54). In 2011, rates increased in all age groups less than 15 years of age compared with 2010, particularly amongst those in the 1–4 year age group whose rate increased by 48% from 212 per 100,000 in 2010 to 314 per 100,000 in 2011. The highest age group rate remained in the 5–9 year age group, 552 per 100,000, a 31% increase compared with the 422 per 100,000 reported in 2010. In contrast, rates decreased amongst all age groups over 15 years of age including a 15% decrease in the 15–19 year age group from 91 per 100,000 in 2010 to 78 per 100,000 in 2011.
Figure 54: Notification rate for pertussis, Australia, 2006 to 2011, by age group
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Vaccination status
Pertussis vaccine effectiveness amongst Australian children has been estimated to range from 82% to 89% with the lower figure representing the cohort of children who would not have been eligible for the 18-month booster dose, which was removed from the NIP in 2003.55 Immunity to disease decreases over time post-vaccination with estimates of protection remaining for 4–12 years.56 The current vaccine schedule for pertussis under the NIP includes a dose provided at 2, 4 and 6 months of age followed by a booster at 4 years of age and again at 12–17 years of age (the timing of this last booster dose varies by jurisdiction). In response to the ongoing epidemic in 2011, some infants were given their first vaccination at 6 weeks of age and their fourth from 3.5 years.
Follow-up is required in order to determine the vaccination status of individual cases. In a large outbreak follow-up of all cases is not possible and as per national guidelines jurisdictions prioritised follow-up to those less than 5 years of age. This age group made up 12.6% (n=4,865) of all notified cases in 2011.
Information on vaccination status was available for 92% (n=4,481) of all cases in children less than 5 years of age; 67% (n=2,989) were fully vaccinated for age, 18% (n=797) were partially vaccinated for age and 11% (n=500) were not vaccinated. Four per cent (n=195) were less than 6 weeks of age and therefore too young to be vaccinated.
Discussion
Pertussis was the most commonly notified vaccine preventable illness in Australia in 2011 reflecting the ongoing epidemic activity across the country in this year. Epidemics of pertussis occur at regular intervals of approximately 3 to 5 years on a background of endemic circulation in Australia.57 The timing of this epidemic activity was not uniform across the country. States and territories experienced peak levels of pertussis at varying intervals as evidenced in 2011 when South Australia had its lowest rate since 2008, while the Australian Capital Territory, New South Wales, Queensland, Victoria and Western Australia all experienced the highest rates since the epidemic began.
In vaccinated populations, outbreaks of pertussis tend to be smaller with less mortality and morbidity than in unvaccinated populations.14 Despite the large number of cases reported in Australia throughout this epidemic period, there does not appear to have been a concurrent increase in pertussis related mortality.58 While pertussis can affect people of any age, infants are at highest risk of more severe disease as adequate immunity is not achieved through infant vaccination until at least the second vaccine dose has been administered at 4 months of age.59 In Australia during this epidemic period, very young un-immunised infants or incompletely immunised children accounted for the majority of severe disease requiring hospitalisation.60
The causes of this epidemic are likely to be multi-factorial. A widespread shift in diagnostic practice associated with the increased use of PCR for pertussis diagnosis in all age groups61,62 and increased case ascertainment during the epidemic period both serve to amplify the number of reported cases. Additional contributory factors may also include waning immunity levels in the vaccinated population including amongst children following their booster vaccination at 4 years of age,63,64 reduced vaccine efficacy of the acellular vaccine compared with the whole cell vaccine,65 the removal of the 18-month dose from the routine schedule66 and adaptation of Bordetella pertussis to the acellular vaccine.67
Strategies to reduce pertussis infection in young children, particularly those less than 6 months of age, continued in 2011. In February 2001, the Australian Technical Advisory Group on Immunisation (ATAGI) endorsed recommendations to bring forward the first dose of the pertussis-containing vaccine from 8 weeks to 6 weeks and schedule the fifth (adolescent booster) dose at 11 to 13 years of age to better protect siblings, especially newborns.68 States and territories continued to provide ongoing public awareness campaigns and most extended funding during 2011 for booster vaccination programs for parents and carers of infants. ATAGI also discussed the United States Centers for Disease Control and Prevention Advisory Committee on Immunization Practices recommendation to vaccinate pregnant women but concluded that while there is indirect evidence that maternal immunisation would be beneficial, further data on safety and efficacy would be required before it could recommend this as a routine option.69
Poliomyelitis
Poliomyelitis is a highly infectious disease caused by gastrointestinal infection by poliovirus. Transmission occurs primarily person-to-person via the faecal-oral route. In most cases poliovirus infection is not symptomatic but in less than 1% of cases the virus may invade the nervous system and cause acute flaccid paralysis (AFP).14
In 2011, there were no notifications of poliomyelitis in Australia, which along with the Western Pacific Region remained poliomyelitis free. Poliomyelitis is a notifiable disease in Australia with clinical and laboratory investigation conducted for cases involving patients of any age with a clinical suspicion of poliomyelitis. Australia follows the WHO protocol for poliomyelitis surveillance and focuses on investigating cases of AFP in children under 15 years of age. The WHO target for AFP surveillance in a polio non-endemic country is 1 case of AFP per 100,000 children aged less than 15 years, which in 2011 Australia achieved for the fourth consecutive year in a row. More details can be found in the annual report of the Australian National Polio Reference Laboratory published in the CDI.
Rubella and congenital rubella
Rubella is generally a mild and self-limiting viral infectious disease. It is spread person-to-person through contact with respiratory secretions directly or via air-borne droplets. Clinically, rubella can be difficult to distinguish from other diseases that cause a febrile rash, such as measles, and is asymptomatic in up to 50% of cases. Rubella infection in pregnancy can result in foetal infection resulting in congenital rubella syndrome (CRS). CRS occurs in up to 90% of infants born to women who are infected during the first 10 weeks of pregnancy and may result in foetal malformations and death.14
Epidemiological situation in 2011
In 2011, there were 58 notifications of rubella; a rate of 0.3 per 100,000 and 1.5 times the notification rate 5-year mean. The increase in cases in 2011 was not associated with any particular outbreak and was likely due to the sporadic nature and overall small number of cases reported annually (Figure 55). There were no cases of CRS reported in 2011. Indigenous status was recorded in 78% of cases, one of which was reported as Indigenous.
Figure 55: Notifications of rubella, Australia, 2006 to 2011, by month of diagnosis
Text version of Figure 55 (TXT 1 KB)
Source of infection
In 2011, a quarter of the cases were reported as being imported from overseas (26%, n=15). The remaining cases (n=43) were reported as being locally acquired with the original source of infection unknown. The majority of imported cases were from Asia, South East Asia (n=9), China (n=3) and India (n=1).
Age and sex distribution
The male to female ratio of notified cases in 2011 was 1.1:1 comprising 30 males and 28 females. Females had higher rates than males between 10 and 29 years of age and in the 60–64 year age group but males predominated in all other age groups (Figure 56). The highest rates for both males and females occurred in the 25–29 year age group, 0.7 per 100,000 and 1.0 per 100,000 for males and females respectively.
Figure 56: Notification rate for rubella, Australia, 2011, by age group and sex
Text version of Figure 56 (TXT 1 KB)
The majority of cases cluster around the young adult age groups with 74% of cases aged between 20 and 49 years of age and a median age of 31 years. The majority (75%) of female cases were notified in women of child-bearing age ranging from 15 to 36 years of age.
In 2011, an increasing trend was evident in the 20–29 year age range where the rate increased from 0.2 per 100,000 in 2009 to 0.7 per 100,000 in 2011, a 176% increase (Figure 57).
Figure 57: Notification rate for rubella, Australia, 2006 to 2011, by age group
Text version of Figure 57 (TXT 1 KB)
Vaccination status
A single dose of rubella vaccine produces an antibody response in more than 95% of recipients and while antibody levels are lower than after natural infection, they are shown to persist for at least 16 years in the absence of endemic disease.44 Rubella vaccine is included in the combined MMR vaccine and provided under the NIP schedule at 12 months and 4 years of age.
Information on vaccination was available for 40% (n=23) of rubella cases, 57% (n=13) of which were reported as not vaccinated and 43% (n=10) as vaccinated. Six of the 10 vaccinated cases were reported as receiving 1 dose of a rubella-containing vaccine and 1 case had reportedly received 2 doses. Dose information was not available for the remaining 3 cases.
Tetanus
Tetanus is an acute, often fatal disease caused by the toxin produced by the bacterium Clostridium tetani. Tetanus spores usually enter the body through contamination of a wound with soil, street dust or animal or human faeces.14 The neurotoxin acts on the central nervous system to cause muscle rigidity with painful spasms. Generalised tetanus, the most common form of the disease, is characterised by increased muscle tone and generalised spasms. Early symptoms and signs include increased tone in the jaw muscles, difficulty in swallowing, stiffness or pain in the neck, shoulder and back muscles. In Australia, tetanus is rare, occurring primarily in older adults who have never been vaccinated or were vaccinated in the remote past.44
Tetanus vaccination stimulates the production of antitoxin, which protects against the toxin produced by the organism. Complete immunisation (3 primary doses and 2 boosters included for children on the NIP) induces protective levels of antitoxin lasting throughout childhood but by middle age, about 50% of vaccinees have low or undetectable levels. It is recommended, though not funded under the NIP, that all adults who reach 50 years of age and have not received a booster of a tetanus-containing vaccine in the previous 10 years should do so.44 Results from the 2006 Adult Vaccination Survey indicate that uptake of this booster vaccine is likely to be low and decrease with increasing age with 67% of adults in the 50–64 year age group (the oldest age group for which data were available) having been vaccinated in the previous 10 years.44
Epidemiological situation in 2011
In 2011, there were 3 notifications of tetanus reported, which was consistent with the low numbers of this disease notified in recent years (Table 2). Because laboratory confirmation of tetanus is usually not possible, notification of cases relies on reports from clinicians, resulting in the potential for under reporting.38 There were 2 male and 1 female cases, aged 84, 18 and 75 years respectively. One case had last been vaccinated 63 years earlier, the 18-year-old was of unknown vaccination status and the remaining case was not vaccinated.
Varicella zoster virus infections
The varicella zoster virus (VZV) is a highly contagious member of the herpesvirus family and causes 2 distinct illnesses: chickenpox (or varicella) following initial infection and shingles (or herpes zoster). Shingles occurs following re-activation of latent virus in approximately 20%–30% of cases, most commonly after 50 years of age.14
In 2006, CDNA agreed to make 3 categories of VZV infection nationally notifiable: chickenpox, shingles and varicella infection unspecified. By 2009 all jurisdictions were notifying VZV to NNDSS with the exception of New South Wales, where VZV is not notifiable.
Epidemiological situation in 2011
In 2011, there were 13,808 notifications of VZV infection from the 7 reporting jurisdictions. This was 16% more than the 11,877 notified in 2010 and continues an upward trend in notifications since 2009. In 2011, 56% (n=7,715) of cases were reported as unspecified varicella infection, 29% (n=3,999) as shingles and 15% (n=2,094) as chickenpox (Figure 58). Although varying by jurisdiction, the VZV unspecified proportion of all VZV notified cases continued its downward trend accounting for 56% of cases in 2011 compared with 60% in 2010 and 62% in 2009.
Figure 58: Proportion of notifications of varicella zoster virus unspecified, chickenpox and shingles, 2011, by state or territory*
* Excluding New South Wales.
Text version of Figure 58 (TXT 1 KB)
Varicella zoster virus infection (unspecified)
Notifications of unspecified VZV infections are laboratory specimens that are positive for VZV but have not been followed up by the local health authority and distinguished clinically as either chickenpox or shingles.
Epidemiological situation in 2011
There were 7,715 notifications of unspecified VZV infections in 2011; a rate of 50 per 100,000 and an 8% increase in notifications compared with 2010.
The highest rate of unspecified VZV was reported from Queensland at 87 per 100,000 (n=4,002) followed by Western Australia and Victoria with 43 per 100,000 each (n=1,007 and n=2,409 respectively). VZV unspecified rates should be interpreted with caution as they are directly dependent on the jurisdictional practice of following-up laboratory notifications.
Age and sex distribution
The male to female ratio in the unspecified VZV notifications was 0.9:1 with females having an overall higher rate of notification with 54 cases per 100,000 compared with 47 per 100,000 in males and predominating across the majority of age groups. The highest rates occurred in the 85 years or over age group for both males, 112 per 100,000, and females, 104 per 100,000. The lowest rates were in the 0–4 year age group, likely reflecting the practice of increased follow up amongst children to determine clinical presentation (Figure 59).
Figure 59: Notification rate for varicella zoster virus infection (unspecified), Australia,* 2011, by age group and sex
* Excluding New South Wales.
Text version of Figure 59 (TXT 1 KB)
Chickenpox
Chickenpox is a highly contagious infection spread by air-borne transmission of droplets from the upper respiratory tract or from the vesicle fluid of the skin lesions of a patient with chickenpox or shingles infection. Chickenpox is usually a mild disease of childhood; however, complications occur in approximately 1% of cases. It is more severe in adults and in individuals of any age with impaired immunity, in whom complications, disseminated disease, and fatal illness can occur.44
Epidemiological situation in 2011
In 2011, there were 2,094 notifications of chickenpox; a rate of 14 per 100,000 and a 20% increase in notifications compared with 2010. The highest rate, 64.2 per 100,000 was reported from the Northern Territory (n=148), followed by South Australia, 29 per 100,000 (n=477) reflecting the increased case ascertainment in these jurisdictions compared with others.
Age and sex distribution
The male to female ratio in 2011 was 1:1 although there was some slight variation, particularly in the older age groups where reported case numbers were smaller. Sixty-three per cent of cases (n=1,328) occurred in children aged less than 10 years. The 5–9 year age group had the highest notification rate amongst both sexes and all age groups, 87 per 100,000 for males and 80 per 100,000 for females (Figure 60). Although higher rates amongst children compared with adults is expected for chickenpox, they also reflect the jurisdictional practice of not following up adult cases.
Figure 60: Notification rate for chickenpox, Australia,* 2011, by age group and sex
* Excluding New South Wales.
Text version of Figure 60 (TXT 1 KB)
Vaccination status
In November 2005, the monovalent varicella zoster vaccine was added to the NIP as a single dose due at 18 months of age (for children born on or after 1 May 2004), or as a catch-up dose at 10–13 years of age. In 2011, children born in 2004 and eligible for the 18-month dose would be 7 years of age or younger and as follow-up of cases does not routinely occur in those older than 7 years, and analysis of vaccination status is restricted to this cohort. Information was available for 51% (n=525) of the 1,028 children less than 8 years of age. Thirty-one per cent (n=165) were vaccinated and 69% were either not vaccinated (n=126) or less than 18 months of age and ineligible for vaccination (n=234).
Shingles
Shingles occurs most commonly with increasing age, impaired immunity, and a history of chickenpox in the first year of life. Reactivation of VZV causing shingles is thought to be due to a decline in cellular immunity to the virus, and in the majority of cases presents clinically as a unilateral vesicular rash in a dermatomal distribution. Associated symptoms may include headache, photophobia, malaise, and itching, tingling, or severe pain in the affected dermatome. In the majority of patients, shingles is an acute and self-limiting disease but complications develop in approximately 30% of cases, the most common of which is chronic severe pain or post-herpetic neuralgia.14
Epidemiological situation in 2011
There were 3,999 notifications of shingles reported to NNDSS in 2011; a rate of 26 per 100,000 and a 34% increase compared with 2010. The highest rates of shingles occurred in South Australia, 97 per 100,000 (n=1,614) and the Northern Territory, 81 per 100,000 (n=186). High rates in these jurisdictions likely reflect their increased case ascertainment compared with others.
Age and sex distribution
There were more female cases (n=2,234) than males (n=1,764); a ratio of 0.8:1. As expected, rates increased with age with the highest rate for males in the 80–84 year age group, 66 per 100,000 and in females in the 85 years or over age group, 73 per 100,000 (Figure 61).
Figure 61: Notification rate for shingles, Australia,* 2011, by age group and sex
* Excluding New South Wales.
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