Results - Part 2 continued

Vaccine preventable diseases

Overview

This section summarises the national surveillance data for notifiable diseases targeted by the National Immunisation Program (NIP) in 2013. These include diphtheria, invasive Haemophilus influenzae type b (Hib) infection, laboratory confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease (IPD), poliomyelitis, rubella, tetanus and varicella zoster infections (unspecified, chickenpox and shingles). 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 reported under the ‘Gastrointestinal’ and ‘Zoonoses’ sections respectively. More detailed reports on historical data, including notifications, hospitalisations and deaths are published in the CDI journal supplements ‘Vaccine Preventable Diseases in Australia’²⁶ and additional analysis on individual diseases are published in CDI in the ‘Australian Vaccine Preventable Diseases Epidemiological Review Series’.

In 2013, there were 59,630 VPD notifications reported to the NNDSS, representing 27% of all reported cases and a 31% decrease compared with 2012 (85,848 cases). Influenza was the most commonly notified VPD with 28,329 cases (48%) reported, followed by pertussis (12,341 cases, 21%). The number of notifications and notification rates for VPDs in Australia are shown in Table 3, Table 4 and Table 5.

Vaccination coverage is an important factor influencing the incidence of VPDs. Since the commencement of the Australian Childhood Immunisation Register in 1996, immunisation coverage in children has been high by international standards, although geographical pockets of lower coverage, in which there is an increased potential for VPD cases, remain. As no vaccine is 100% effective, infections with these diseases sometimes do occur in fully vaccinated people, and some are reported later in this section. However, vaccines do provide a substantially lower chance of becoming infected or will reduce the severity of disease.

Information on a case’s vaccination history was previously recorded in the NNDSS using the ‘vaccination status’ field (fully or partially vaccinated for age or not vaccinated), plus fields capturing the number of doses, the last vaccination date and how the vaccination information was validated. In January 2008 new, more detailed fields were incorporated for recording ‘vaccine type’, and ‘vaccination date’ for each dose of vaccine given. The new fields were intended to replace the old fields, with a transition period allowing either field to be utilised. In 2013, all jurisdictions were using the new fields except for the Australian Capital Territory. In this report the vaccination status of a case is interpreted according to the data provided by the states and territories from the 2 different formats. A case is described as fully vaccinated if they have received all doses of the relevant vaccine according to the most recent edition of The Australian Immunisation Handbook⁵⁰ and at least 14 days prior to disease onset. In contrast, fully vaccinated for age describes a case that has received all recommended doses of a vaccine for their age but may not yet have received the full course of vaccinations required to be considered fully vaccinated.

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In 2013, the measles-mumps-rubella-varicella (MMRV) vaccine for all children at 18 months of age and the combined Hib and monovalent meningococcal C conjugate vaccine (Hib-MenCCV) for all children at 12 months of age were added to the NIP. The MMRV replaced the 2nd dose of MMR previously provided at 4 years of age and combined it with the varicella vaccine already given at 18 months of age. This change is expected to provide earlier protection and improve coverage of the second dose of MMR while being consistent with the World Health Organization (WHO) recommendation that a 2nd dose of measles containing vaccine should be given in the 2nd year of life.⁵¹ Hib-MenCCV replaces the single dose of MenCCV and booster dose of monovalent Hib vaccine previously scheduled at 12 months of age.⁵⁰

Diphtheria

• There were 2 cases of diphtheria notified in Australia in 2013.
• Diphtheria is now rare in Australia.

Diphtheria is an acute pharyngeal or cutaneous infection caused mainly by toxigenic strains of Corynebacterium diphtheriae. The exotoxin acts locally on the mucous membranes of the respiratory tract, and on damaged skin, although this is not as common. Disease is mainly due to local membranous inflammation, which for pharyngeal diphtheria can cause airway obstruction. Occasionally, systemic infections occur and cause damage to the myocardium, nervous system and kidneys. Diphtheria is spread by respiratory droplets or direct contact with nasopharyngeal secretions or skin lesions. While there are non-toxigenic strains of C. diphtheriae, they usually only cause mild throat or skin infection and are not nationally notifiable.²¹

Epidemiological situation in 2013

In 2013, there were 2 notifications of diphtheria reported to the NNDSS, one from Queensland and one from South Australia. Both cases were imported infections from Papua New Guinea and India respectively.

Diphtheria is rare in Australia, with most cases associated with sporadic importations from countries in which this disease remains endemic. Since the 1 case of cutaneous diphtheria reported in 2001, the only other year before 2013 in which cases were reported was 2011, when a cluster of 3 infections, including 1 death, and an unrelated case of cutaneous diphtheria were notified.

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Influenza

• In 2013, notifications of laboratory confirmed influenza decreased by almost 37% from 2012 making it a mild to moderate season since the 2009 pandemic season.
• Children aged 9 years or under, and also middle aged adults, as well as those with underlying medical conditions were most affected.

Influenza is a common, highly infectious acute respiratory disease caused by infection with influenza viruses. The virus is transmitted from person to person by airborne droplets of exhaled respiratory secretions, especially by coughing or sneezing.⁵² The disease caused by infection with influenza viruses ranges from asymptomatic⁵³ through to mild upper respiratory tract illness, to severe complications including pneumonia. The severity of disease is determined by features intrinsic to the virus including its similarity to previous circulating and vaccine strains and by host factors including the presence of chronic conditions, pregnancy and smoking in the population.⁵⁴ The goals of influenza surveillance are to determine the magnitude and distribution of illness, detect outbreaks, monitor for changes in the virus and to facilitate policy development and planning.⁵⁵

Annual influenza vaccination is the primary means of preventing or attenuating influenza and its complications and is included in the NIP for individuals who are at increased risk of complications from influenza infection. In 2013, the NIP funded influenza vaccine for people aged 6 months or over with medical conditions placing them at risk of serious complications due to influenza, Aboriginal and Torres Strait Islander people aged 15 years or over, pregnant women and people aged 65 years or over.

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Epidemiological situation in 2013

In 2013, there were 28,329 cases of laboratory confirmed influenza, which was almost two-thirds the number of notified cases reported in 2012, but similar to the number of cases notified in 2011.

Geographic distribution

Notification rates were highest in South Australia (289 per 100,000) and the Northern Territory (199 per 100,000). Notifications in the Australian Capital Territory, New South Wales, Queensland, Victoria and Western Australia were somewhat similar to the national notification rate of 123 per 100,000, while the Tasmanian rate was substantially lower than the national rate at 58 per 100,000. New South Wales reported the highest number of influenza cases of any jurisdiction, comprising 30% of all notifications, which differed from previous seasons, when Queensland reported the highest number (Figure 36).

Figure 36: Notified cases of laboratory confirmed influenza, Australia, 2013, by week and state or territory

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Age and sex distribution

The highest number of influenza notifications occurred in the 0–4 years and 5–9 years age groups, which together accounted for 22% of all notifications (Figure 37).

Figure 37: Notified cases of laboratory confirmed influenza, Australia, 2013, by age group and sex*

* Excludes 35 notifications for which age or sex was not reported.

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Likewise, notification rates were highest in the 0–4 years and 5–9 years age groups (214 and 213 notifications per 100,000 respectively) (Figure 38). There were also higher notification rates seen in middle aged adults (35–39 years and 40–44 years age groups).⁵⁶

Figure 38: Notification rate for laboratory confirmed influenza, Australia, 2008 to 2013, by age group and year

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In seasons dominated by the influenza A(H1N1)pdm09 virus, such as 2009, 2010 and 2011, the age distribution of influenza notifications showed a downward trend with increasing age. For comparison, in 2012, which was dominated by influenza A(H3N2), the age distribution of influenza notifications was bimodal with peaks in those aged under 10 years and in those aged 70 years or over, and a small peak among those aged 30–44 years. The 2013 influenza season has been characterised by co-circulation of A(H1N1)pdm09, influenza A(H3N2) and influenza B viruses.

In 2013, females accounted for 15,033 (53%) of the influenza notifications for which sex was reported. Notification rates per 100,000 were generally higher among females in the adult age groups, whereas males dominated the younger age groups (0–14 years).

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Seasonality

Influenza notification activity during the 2012–13 inter-seasonal period was the 2nd highest on record behind that observed during the 2010–11 inter-seasonal period. Excluding 2010, notifications of influenza in 2013 started their seasonal increase later, and rose and peaked moderately in comparison with previous years (Figure 39).

Figure 39: Notified cases of laboratory confirmed influenza, Australia,* 2008 to 2013, by month and year

* In South Australia, influenza was not made notifiable through legislation until May 2008.

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The majority of jurisdictions peaked in activity around late August, followed by a decline in influenza activity back to inter-seasonal levels. However, influenza activity remained particularly elevated in South Australia, Queensland and the Northern Territory during the latter part of 2013

Indigenous status

Of those states where Indigenous status completeness was greater than 50% (Western Australia, South Australia and the Northern Territory), the age standardised notification rate for influenza was 265 per 100,000 in the Indigenous population and 163 per 100,000 for the non-Indigenous population, representing a rate ratio of 1.6:1.

Mortality

Nationally, there were 48 influenza-associated deaths notified to the NNDSS, with a median age of 67 years (range 27–97 years). The majority of deaths were associated with influenza A infections (n=39; 81%), and of these, 16 were associated with A(unsubtyped) infections, 16 were A(H3N2) and seven were A(H1N1)pdm09. Indigenous status was reported for 75% (n=36) of the influenza-associated deaths; and Indigenous peoples accounted for 8% (n=3) of these deaths. The number of influenza-associated deaths reported to the NNDSS is reliant on the follow-up of cases to determine the outcome of their infection and most likely underestimates the true mortality impact associated with this disease.

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Microbiological trends

In 2013, typing data was reported for all but 11 laboratory confirmed influenza notifications. Of notifications with typing information, 63% were type A (43% A(unsubtyped), 14% (H1N1)pdm09 and 6% (H3N2) and 37% type B. Mixed influenza type A and B infections accounted for <1% of notifications. None were reported as influenza type C (Figure 40).

Figure 40: Notified cases of laboratory confirmed influenza,* Australia, 2013, by week and subtype

* Excludes 77 mixed type A and B, and untyped influenza infections.

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The overall type breakdown was similar in 2011 and 2012. Whilst the majority of influenza A reports are unsubtyped, 14% of overall notifications were reported as influenza A(H1N1)pdm09, compared with less than 1% in 2012. Further, the proportion of influenza B notifications reported in 2013 has been higher than in previous years.

For 2013, the WHO Collaborating Centre for Reference and Research on Influenza (WHOCC) analysed 1,570 specimens from Australian influenza cases. This represented approximately 6% of the 28,329 laboratory confirmed cases reported to the NNDSS. Influenza A(H1N1)pdm09 comprised 45% (n=699) of influenza viruses followed by influenza B (39%; n=613) and influenza A(H3N2) (16%; n=258) (Figure 41).

Figure 41: World Health Organization Collaborating Centre for Reference and Research on Influenza subtyped influenza virus samples, Australia, 2012 and 2013

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The WHOCC assessed the antigenic similarity of circulating influenza virus isolates to reference strains by haemagglutination inhibition (n=1,532 influenza virus isolates). All of the A(H1N1)pdm09 isolates (n=688) were antigenically similar to the A/California/7/2009 vaccine virus, with 5% (n=35) characterised as ‘low reactors’. The haemagglutinin of these low reactor viruses mostly contained amino acid substitutions acquired in vitro as a result of adaptation to growth in Madin-Darby canine kidney cells as these changes were not present in the original clinical samples. All of the A(H3N2) isolates (n=234) were antigenically similar to the A/Victoria/361/2011 vaccine virus.

Of the influenza B viruses (n=610), 96% were from the B/Yamagata lineage, with the remainder from the B/Victoria lineage. Of the B/Yamagata lineage viruses (n=583), almost all were B/Massachusetts/2/2012-like viruses (n=580), including a few ‘low reactors’ (n=7), with the remaining B/Yamagata lineage viruses (n=3) characterised as low reactor B/Wisconsin/1/2010-like viruses. The small number of B/Victoria lineage viruses (n=27) were all antigenically similar to the former vaccine strain B/Brisbane/60/2008.

Of the viruses included in the 2013 trivalent Australian influenza vaccine, the influenza A(H1N1)pmd09 and A(H3N2) viruses that were isolated during 2013 were antigenically similar to the 2013 vaccine viruses. However, the B/Yamagata lineage virus isolates were mostly antigenically similar to the B/Massachusetts/2/2012 virus, with very few detections of the B/Wisconsin/1/2010 vaccine strain.

Viruses collected in 2013 were also tested for sensitivity to the neuraminidase inhibitor class of antiviral drugs. Neuraminidase inhibition assays were performed on 1,458 virus isolates consisting of 665 A(H1N1)pdm09, 575 B and 218 A(H3N2) viruses. Reduced inhibition by oseltamivir was detected in 4 A(H1N1)pdm09 isolates and was mediated by the well characterised H275Y mutation, which is known to confer resistance to oseltamivir.⁵⁷ Reduced inhibition to zanamivir was detected in a single B/Yamagata lineage isolate.

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Enhanced surveillance data sets

In addition to NNDSS data, a series of targeted influenza surveillance systems operated during 2013. Together, these systems collected data that were used to describe the season under the areas of epidemiology, morbidity, mortality and virology and supported the conclusions drawn from analyses of NNDSS notification data. Enhanced influenza surveillance was based on the following additional sources of data:

• the number and proportion of calls to a national health call centre network for influenza or influenza-like illness (ILI);
• rates of ILI from a community survey;
• consultation rates for ILI identified by sentinel general practitioners;
• consultation rates for ILI identified by hospital emergency departments in Western Australia, New South Wales and the Northern Territory;
• hospitalised cases of influenza from 15 sentinel hospitals across Australia;
• mortality data from the New South Wales Registry of Births, Deaths and Marriages; and
• typing and subtyping for influenza from sentinel laboratories in New South Wales, Victoria, Western Australia and Tasmania.

These data sources were used to inform the overall picture of influenza activity in Australia and comprehensive analysis of these data are provided in the fortnightly Australian Influenza Surveillance Report, which was published during the influenza season, and in the annual National Influenza Surveillance Scheme report.

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Discussion

The 2013 influenza season in Australia began in early July, peaked in late August and was largely concluded by mid-December. Australia experienced sustained virus circulation until mid-October, which continued until mid-December for South Australia, Queensland and the Northern Territory in particular. Peak NNDSS notifications occurred approximately 1 month later than the median week of peak transmission for 2012.⁵⁸ The most commonly detected virus was influenza A(H1N1)pdm09, however influenza type B and A(H3N2) were also prominent. The age distribution of influenza notifications in the 2013 season was mixed, with infants and young children most affected, followed by middle-aged adults.

Taken together, data from most influenza surveillance systems showed that the overall impact of influenza in 2013 was indicative of a relatively mild to moderate season with some sustained activity experienced in the latter part of the year. The average number of influenza notifications reported per week during the season were around half that in 2012, and both ILI and influenza activity across systems were overall lower than in 2012.⁵⁹

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Invasive Haemophilus influenzae type b

• There were 20 cases of invasive Hib reported in 2013.
• Of the cases reported 60% were female and 55% were under the age of 5 years.
• The 2013 notification rate of Hib remains low at 0.1 per 100,000 population.

Invasive Hib is a bacterium that causes disease with symptoms dependant on which part of the body is infected. These include: septicaemia (infection of the blood stream); meningitis (infection of the membranes around the brain and spinal cord); epiglottitis (severe swelling of the epiglottis at the back of the throat); pneumonia (infection of the lungs); osteomyelitis (infection of the bones and joints) and cellulitis (infection of the tissue under the skin, usually on the face).

Since the introduction of the Hib vaccine on to the NIP in 1993, there has been a reduction of more than 95% in notified cases of Hib disease in Australia, which now has one of the lowest rates in the world.²⁶

Epidemiological situation in 2013

In 2013, there were 20 notifications of Hib disease reported. This was a slight increase compared with cases reported in 2012 (n=15), and representing a ratio of 1.0 compared with the mean of the previous 5 years. The 2013 notification rate was 0.1 per 100,000 and was consistent with the very low rates seen since the introduction of the vaccine on the NIP in July 1993 (Figure 42).

Figure 42: Notified cases and notification rate for invasive Haemophilus influenzae type b infection, Australia, 1993 to 2013, by year of diagnosis

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Cases occurred in the 3 most populous states of New South Wales (n=9), Queensland (n=7) and Victoria (n=4). The notification rates were consistent between states ranging from 0.1 per 100,000 in Victoria to 0.2 per 100,000 in Queensland. There were no infants deaths reported in 2013. One Hib associated death was reported in a 65-year-old non-Indigenous female of unknown vaccination status.

Age and sex distribution

In 2013, the male to female ratio was 0.7:1, 8 male and 12 female cases. More than half of the cases (n=11) were in children aged less than 5 years and 73% (n=8) of these were among infants less than 1 year. Consistent with previous years, the 0–4 years age group had the highest notification rate (0.7 per 100,000). There were no cases reported among young adults between 20 and 39 years of age while adults 40 years of age or over accounted for 35% (n=8) of cases (Figure 43).

Figure 43: Notification rate for invasive Haemophilus influenzae type b infection, Australia, 2013, by age group and sex

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Indigenous status

Indigenous status was reported for 90% (n=18) of all cases in 2013. Two cases were reported as being Indigenous, representing a notification rate of 0.3 per 100,000, which was consistent with 2012 and 2011 (0.3 per 100,000 and 0.4 per 100,000 respectively) and lower than 2010 (1.4 per 100,000).

Vaccination

The NIP schedule in 2013 recommended a primary course of 3 doses at 2, 4, and 6 months of age, with additional booster doses at 4 years and between 10 and 15 years, delivered through school-based programs.⁵⁰

In 2013, persons aged less than 21 years of age were eligible for Hib vaccination under the NIP during their infancy. Twelve of the 20 Hib cases reported in 2013 were eligible for vaccination. Of the 5 cases who were 12 months of age or over and therefore eligible for the full vaccine course, none were fully vaccinated. Of the 7 cases who were less than 12 months of age, six were partially vaccinated and one was not vaccinated. Two partially vaccinated cases had received all 3 primary vaccine doses, two had received 2 doses and two had received 1 dose.

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Invasive pneumococcal disease

• A total of 1,546 cases of invasive pneumococcal disease were notified in 2013, representing a notification rate of 6.7 per 100,000.
• This was the lowest national rate reported since the introduction of the universal 7-valent pneumococcal conjugate vaccine (7vPCV) program for young children in 2005 and follows the replacement of the 7vPCV with the 13-valent pneumococcal conjugate vaccine (13vPCV) in July 2011.

Invasive pneumococcal disease is a disease in which Streptococcus pneumoniae is isolated from a normally sterile site such as blood, cerebrospinal fluid or pleural fluid. Transmission of the bacterium from person to person is usually via the inhalation of infected respiratory droplets. Many of the signs and symptoms of IPD are non-specific including fever, chills, headache, stiff neck and a general feeling of being ‘out-of-sorts’, through to seizures and occasionally coma.

Epidemiological situation in 2013

There were 1,546 notified cases of IPD reported in 2013, representing a notification rate of 6.7 per 100,000. This was the lowest national rate reported since the introduction of the universal 7vPCV program for young children in 2005.

Geographic description

The number of cases in all states and territories, except for Victoria, decreased in 2013 with the Australian Capital Territory recording the greatest reduction in cases (48% decrease) when compared with 2012. The notification rate of IPD varied from 3.7 per 100,000 in the Australian Capital Territory to 24.0 per 100,000 in the Northern Territory. Victoria recorded only a small increase in the number of cases notified, maintaining the same rate as recorded in 2012 (6.8 per 100,000).

Age and sex distribution

In 2013, males accounted for 54% (n=829) of cases of IPD, resulting in a male to female ratio of 1.2:1. The rate for disease in males exceeded that in females in all age groups except for the 25–29, 50–54, 55–59 and 60–64 years age groups (Figure 44).

In 2013, the notification rate for IPD was highest in the elderly and in young children, with an age distribution similar to the distribution seen in 2012. In the elderly, the highest notification rate was in those aged 85 years or over (31.4 per 100,000), while the highest rate in children aged less than 5 years was in those aged 1 year (21.4 per 100,000) (Figure 44).

Figure 44: Notification rate for invasive pneumococcal disease, Australia, 2013, by age group and sex

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Seasonality

Many respiratory diseases including IPD are known to show a distinct seasonal trend that generally peaks during the winter months. In 2013, the seasonal trend of IPD was consistent with previous years with notifications peaking in August (n=230) (Figure 45).

Figure 45: Notified cases of invasive pneumococcal disease, Australia, 2008 to 2013, by month of diagnosis

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Indigenous status

Completeness of Indigenous status reporting was reasonable in 2013, with 88% (n=1,356) of cases reported with a known Indigenous status. Of those cases with a known Indigenous status, 14% (n=193) of notifications were reported as Indigenous. In 2013, the notification rate for IPD in the Indigenous population (32.1 per 100,000) was approximately 6 times the rate for non-Indigenous people (5.2 per 100,000). In 2013, the notification rate for IPD in the non-Indigenous population was the lowest recorded since the introduction of the universal 7vPCV program for young children in 2005 (Figure 46).

Figure 46: Notification rate for invasive pneumococcal disease, Australia, 2003 to 2013, by Indigenous status, year of diagnosis and age group

2005 – Introduction of universal childhood 7vPCV immunisation program.

July 2011 – The 13vPCV immunisation replaced the 7vPCV component in the universal childhood immunisation program.

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In 2013, the notification rate for IPD in Indigenous children aged under 5 years (36.1 per 100,000) reached its lowest since 2005. The rate in non-Indigenous children aged under 5 years (10.8 per 100,000) only slightly exceeds the lowest rate recorded in this subgroup since 2005 (10.5 per 100,000 in 2012).

Vaccination

In Australia, pneumococcal vaccination is recommended as part of routine immunisation for the medically at-risk, children under 5 years of age, Aboriginal and Torres Strait Islander peoples aged 50 years or over and other Australians aged 65 years or over.⁵⁰

The 7vPCV was added to the NIP schedule in 2001 for Indigenous and medically at-risk children and then expanded in 2005 to include all infants nationally, together with a catch-up vaccination for all children aged less than 2 years. In 2011, the 7vPCV was replaced on the NIP by the 13vPCV and further expanded to include all children aged under 5 years. The 7vPCV targets 7 S. pneumoniae serotypes (4, 6B, 9V, 14, 18C, 19F and 23F) and the 13vPCV targets the same 7 serotypes plus 6 additional serotypes (1, 3, 5, 6A, 7F, 19A). In 2013, 37% of notifications in children aged under 5 years were a result of a serotype included in either the 7vPCV or 13vPCV vaccines.

Vaccination with the 23-valent pneumococcal polysaccharide vaccine (23vPPV) was added to the NIP for Indigenous Australians aged 50 years or over in 1999 and for non-Indigenous Australians aged 65 years or over from January 2005.⁶⁰ The 23vPPV targets 23 S. pneumoniae serotypes (1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19A, 19F, 20, 22F, 23F and 33F). In 2013, 63% of notifications in Indigenous peoples aged 50 years or over, and 59% of notifications in non-Indigenous Australians aged 65 years or over, were a result of a serotype included in 23vPPV.

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Microbiological trends

Although there are over 90 S. pneumoniae serotypes, a relatively limited number cause the majority of IPD. Data on serotypes of pneumococcal isolates is critical for understanding of vaccine effects in both immunised and non-immunised populations such as herd immunity effects and serotype replacement. IPD serotypes were reported in 96% (n=1,491) of notified cases in 2013. The dramatic reduction in IPD due to serotypes targeted by the 7vPCV, following the introduction of the vaccine, in children aged under 5 years has been maintained, although the rate for IPD in Indigenous children aged under 5 years increased from 1.4 per 100,000 (n=1) in 2012 to 5.3 per 100,000 (n=4) in 2013 (Figure 47). This is likely to be a sporadic increase in this group as all 4 cases were caused by a different serotype (14, 18C, 19F and 9V). In 2013, the 7vPCV serotypes accounted for only 7% (n=12) of IPD notifications with known serotype in children aged under 5 years.

Figure 47: Notification rate for invasive pneumococcal disease in children aged less than 5 years, Australia, 2002 to 2013, by Indigenous status, year and serotype category

2001 – Introduction of 7vPCV immunisation for Aboriginal and Torres Strait Islander and medically at-risk children and 23vPPV booster for Aboriginal and Torres Strait Island children in the Northern Territory, Western Australia, South Australia and Queensland.

2005 – Introduction of universal childhood 7vPCV immunisation program.

July 2011 – The 13vPCV immunisation replaced the 7vPCV component in the universal childhood immunisation program.

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Enhanced surveillance data sets

Enhanced data are available for IPD notifications. Further analyses, including risk factors and antibiotic susceptibilities can be found in the IPD annual report series also published in CDI.

Prior to 2011, an increasing trend in IPD due to the 6 additional serotypes targeted by the 13vPCV (13vnon7v), indicative of serotype replacement, was observed in children under 5 years of age. However, since the introduction of the 13vPCV in 2011, the rate for IPD due to the 13vnon7v serotypes in both Indigenous children and non-Indigenous children has reduced to the lowest rate recorded in a decade (5.3 per 100,000 and 3.5 per 100,000 respectively). Overall in 2013, 13vnon7v serotypes accounted for 31% (n=58) of IPD notifications in children aged under 5 years compared with 44% (n=82) in 2012. For both Indigenous and non-Indigenous children, the most common 13vnon7v serotype causing disease in 2013 was still serotype 19A: 100% of cases in Indigenous children and 61% of cases in non-Indigenous children.

Measles

• In 2013, there were 158 notified cases of measles, the majority of which were either imported or import-related.
• There were 20 clusters of two or more epidemiologically linked cases in 2013.
• Transmission was interrupted quickly in all except 1 outbreak involving 44 cases over 17 weeks.
• Of cases eligible for vaccination, the majority were either not vaccinated (43%) or their vaccination status was not able to be established (38%).

Measles is a highly infectious, acute viral illness spread by respiratory secretions, including aerosol transmission.⁶¹ Initial symptoms last 2 to 4 days and are characterised by fever and malaise, followed by a cough, coryza and conjunctivitis. It is usually followed by a red blotchy rash, which typically begins on the face, and then becomes generalised. Measles is often a severe disease with complications more common in the chronically ill, including otitis media, pneumonia, diarrhoea and acute encephalitis.⁶² Subacute sclerosing panencephalitis is a late, rare (approximately 1 in 100,000 cases) complication of measles caused by persistent infection and is always fatal.⁵⁰ Complications are more common in children under 5 years of age and in adults over 20 years of age.⁶³

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Epidemiological situation in 2013

In 2013, there were 158 notifications of measles. This represents a notification rate of 0.7 per 100,000, which is 1.3 times the mean of the previous 5 years but a decrease compared with 2012 and 2011, where 199 and 194 cases were reported respectively (Figure 48).

Figure 48: Notified cases and notification rate for measles, Australia, 1998 to 2013, by year

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Geographic description

In 2013, cases of measles occurred in all states and territories, except the Northern Territory and Tasmania. The majority of cases occurred in Queensland (n=52), followed by Victoria (n=41), New South Wales (n=34), South Australia (n=16), Western Australia (n=14) and the Australian Capital Territory (n=1) (Figure 49).

Figure 49: Notified cases of measles, Australia, 2008 to 2013, by month of diagnosis and state and territory

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Age and sex distribution

The overall male to female ratio was 1.3:1 in 2013, representing a male rate for 0.8 per 100,000 compared with a female rate for 0.6 per 100,000. There was a wide variation in the male to female rate ratio across the age groups with 3 times as many males compared with females in the 25–29 years age group (n=13 and n=4 respectively) and equal numbers in the 0–4 years age group (n=10) (Figure 50)

Figure 50: Notification rate for measles, Australia, 2013, by age group and sex

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In 2013, age at diagnosis ranged from 0 to 51 years with a median age of 21 years. Notification rates decreased or remained consistent across all age groups in 2013, compared with 2012. Consistent with recent years, infants less than 1 year of age had the highest age specific rate, 2.3 per 100,000, in 2013. Rates have remained below 2.5 per 100,000 in all age groups between 2008 and 2013, with the exception of the less than 1 year age group in 2011 and 2012 (Figure 51).

Figure 51: Notification rate for measles, Australia, 2008 to 2013, by year of diagnosis and selected age groups

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Twenty-three cases occurred in those born between 1978 and 1982 (31–35 years of age in 2013), a cohort previously identified as susceptible to measles infection.⁶⁴ One case was born before 1966, a cohort that is considered to have high levels of natural immunity.⁶⁵

Seasonality

In Australia, a seasonal pattern is no longer evident due to the virus no longer being endemic (Figure 49). In temperate climates and where measles transmission remains endemic, the majority of cases occur in late winter to early spring.⁶⁶

Indigenous status

Indigenous status was completed for 91% of cases in 2013 (n=143), a decrease compared with the 98% of cases in 2012. Of these cases, 2.1% (n=3) were reported as Indigenous.

Source of infection and outbreaks

Sixty-four per cent of cases in 2013 were either imported (n=52) or import-related (n=49) with the remaining 36% (n=57) of unknown source (Figure 52).

Figure 52: Notified cases of measles, Australia, 2013, by diagnosis week ending and source of infection

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Of the imported cases, 65% (n=34) were from the WHO defined South East Asia Region, the majority of which were from Indonesia (n=20). The WHO Western Pacific Region, of which Australia is a part, accounted for 17% (n=9) of imported cases. The remaining 18% from the WHO Eastern Mediterranean Region (n=4) and the European Region (n=5).

There were 20 clusters of two or more epidemiologically linked cases in 2013 accounting for 75% (n=119) of all cases. The remaining 25% of cases comprised sporadic imported cases (n=32) and sporadic cases acquired in Australia of unknown source (n=7). The majority of clusters were import related (n=17) comprising 58% (n=69) of cluster cases. The 3 clusters of locally-acquired cases of unknown source occurred in 3 separate states including Western Australia: 1 cluster of 2 cases; New South Wales: 1 cluster of 4 cases; and the large outbreak involving both Victoria and Queensland (n=44 cases).

Transmission was interrupted quickly in all except 1 outbreak. The median duration was 18 days (range 1–118 days) between the onset of symptoms in the index and the last case and the median numbers of generations⁶⁷ was 2 (range 0–12). Nineteen of 20 clusters had less than 10 cases with a median of 3.5 (range 2–44) cases. The largest outbreak, comprising 44 cases, commenced in Victoria (n=7) with subsequent linked cases in Queensland (n=37). This outbreak lasted approximately 17 weeks from the end of July and included 12 generations of spread. While it was classified as being of unknown source, it was most likely associated with an imported case at an international gaming convention in Melbourne, which the index case had attended during the exposure period.

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Vaccination

Two doses of the measles containing vaccine are recommended for all persons born during or after 1966. The MMR induces long term measles immunity in 95% of recipients after a single dose and 99% of recipients after the 2nd dose.⁵⁰

Of the 158 cases notified in 2013, 95% (n=150) were born after 1965 and were 12 months of age or over and therefore eligible for at least 1 dose of a publicly funded measles-containing vaccine. Over 80% of cases eligible for vaccination were either not vaccinated (43%, n=65) or of unknown vaccination status (38%, n=57). Of the remaining 19% (n=28) who were vaccinated, four had received the full course of 2 doses of a measles-containing vaccine and 24 were partially vaccinated with 1 dose (Figure 53).

Figure 53: Notified cases of measles, Australia, 2013, by selected age groups and vaccination status

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The 5–9 years age group had the highest proportion of unvaccinated cases (18%) with young children and adolescents between 5 and 19 years of age accounting for 51% of all unvaccinated cases. The proportion of cases with unknown vaccination status increases with age and where provided may be less reliable mostly being based on self-reporting. In 2013, there was 1 case less than 15 years of age reported as of unknown vaccination in contrast to 44% (n=48) of cases 15 years or over having unknown vaccination status (Figure 53).

Microbiological trends

Genotyping data were available for all 20 clusters with 2 or more linked cases in 2013. Genotype D9 was associated with 7 separate clusters (n=32 cases), D8 with 8 clusters (n=28 cases), B3 with 3 clusters (n=15 cases) and G3 with the large outbreak across Victoria and Queensland (n=44 cases) (Figure 54). Of the 39 sporadic cases 72% (n=28) were genotyped.

Figure 54: Measles clusters, Australia, 2013, by state or territory, genotype and source of infection

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MJO = multi-jurisdictional outbreak

Imported genotypes varied by WHO region. A single genotype was imported from 2 regions; 4 separate importations of B3 from the Eastern Mediterranean Region and 3 separate importations of D8 from the European Region. Multiple genotypes were imported from the South East Asia Region (B3, D8, D9 and G3) and the Western Pacific Region (B3, D8 and D9).

Discussion

The increasing prevalence of measles in some parts of the world and the continued circulation of the virus in countries of close geographical proximity to Australia will result in a continual source of imported virus in Australia. This was particularly the case in 2013 with 52 separate importations occurring. Despite this large number of importations in 2013, the majority were sporadic and did not lead to ongoing local transmission.

Evidence suggests that endemic measles has been eliminated from Australia, since at least 2005.⁶⁶ Based on the WHO definitions, Australia has continued to maintain this status. In 2013, none of the outbreaks persisted for more than 12 months and there was no evidence of a single genotype continuously circulating. Ongoing evidence of high population immunity was demonstrated by the small number of cases and the short duration of outbreaks. Only 1 outbreak in 2013 involved more than 4 generations of transmission, or lasted greater than 6 weeks.

However, due to the highly infectious nature of measles, local transmission and outbreaks will continue to occur, mostly among susceptible contacts of non-immune travellers from countries where measles remains prevalent.

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Mumps

• The mumps notification rate has been less than 1 per 100,000 since 2009.
• In 2013 there were 217 notified cases of mumps.

Mumps is an acute viral illness with an incubation period of 12 to 25 days. Transmission is usually by respiratory secretions, including aerosol transmission, or by direct contact with saliva. Asymptomatic infections occur in one-third of cases. Symptomatic disease ranges from mild upper respiratory tract infections to systemic involvement. The characteristic bilateral, or occasionally unilateral, parotid swelling occurs in 60% to 70% of clinical cases, however a high proportion have non-specific symptoms including fever, headache, malaise, myalgia and anorexia.⁶⁸ Mumps encephalitis has been estimated to occur in 1 to 2 per 10,000 cases, with a case fatality rate of around 1%.

Epidemiological situation in 2013

In 2013, there were 217 notifications of mumps. A notification rate of 0.9 per 100,000, which represented an 8.5% increase compared with the 200 cases reported in 2012 and continues the slight upward trend noted since 2011 (Figure 55). From 2007 to 2010 the overall notification rate of mumps declined, falling from a peak of 2.8 per 100,000 in 2007 to 0.4 per 100,000 in 2010.

Figure 55: Notified cases of mumps, Australia, 2008 to 2013, by month of diagnosis and state or territory

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Geographic description

Cases were reported from all states and territories. Jurisdictional specific rates were highest in the Northern Territory (2.5 per 100,000) followed by Western Australia (1.8 per 100,000).

Age and sex distribution

In 2013, the overall male to female ratio was 1.4:1, with some variation in this ratio between age groups. The highest rates for males occurred in the 15–19 years age group at 2.5 per 100,000, while for females rates were highest in the 40–44 years age group at 1.4 per 100,000 (Figure 56).

Figure 56: Notification rate for mumps, Australia, 2013, by age group and sex

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There were cases of mumps notified across all age groups with the median age at diagnosis being 32 years (range 0–90 years). Consistent with recent years, young adults in the 30–39 and 20–29 years age groups had the highest rates of infection with 1.6 per 100,000 and 1.4 per 100,000 respectively. The most notable increase in age group rates occurred among children less than 1 year of age (Figure 57).

Figure 57: Notification rate for mumps, Australia, 2008 to 2013, by year of diagnosis and selected age groups

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Indigenous status

A known Indigenous status was reported for 79% (n=171) of mumps cases in 2013. This was higher than the level of completeness over the previous 5-year period (mean 63%, range 51% to 77%). Of the cases with a known Indigenous status reported, 5 cases (3%) were reported as Indigenous. The proportion of mumps notifications reported as Indigenous has been less than 5% since 2010.

Outbreaks

Place of acquisition was complete for 74% (n=160) of cases in 2013 of which 18% were imported from overseas: 21 from Asia, five from Europe, two from the Americas and one from Africa. Eighty-two per cent were reported as locally acquired in Australia.

The outbreak reference field was completed for 6% (n=13) of cases in 2013. There were 6 outbreaks of two or more epidemiologically linked cases, all of which occurred in Western Australia. Two of these outbreaks were linked to imported cases.

Vaccination

The mumps vaccine was first funded on the NIP schedule in 1982 for infants at 12 months of age, with those born after 1980 eligible for at least 1 dose of a mumps-containing vaccine.

The mumps component of the MMR vaccine is considered to be the least effective of the 3 components with 1 dose vaccine effectiveness varying between 60% and 90%.^69–71 While protection is greater in 2-dose vaccine recipients, recent outbreaks have been reported among these, particularly young adults who received their vaccines more than 10 years previously.^72,73 Reduced effectiveness of the mumps vaccine over time may also partially account for the proportion of vaccinated cases and contribute to mumps outbreaks in older vaccinated populations.⁷⁴

Of the 217 cases in 2013, 50% (n=109) were eligible for at least 1 dose of a publicly funded mumps-containing vaccine. Of these, 12% (n=13) were unvaccinated and 50% (n=54) were of unknown vaccination status. Of the remaining 38% of cases (n=42), 18 were fully vaccinated, having received 2 doses of a mumps-containing vaccine, 22 were partially vaccinated with 1 dose of a mumps-containing vaccine and 2 cases had no dose number information provided.

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Pertussis

• Pertussis is the least well controlled of all VPDs and remains highly prevalent in Australia.
• In 2013 there were 12,341 cases of pertussis reported, representing a notification rate of 106 per 100,000 population and continuing the downward trend in annual notifications since 2011.
• In 2013, children under 15 years of age had a notification rate 2.7 times higher compared with those 15 years of age or over.

Pertussis, commonly known as whooping cough, is a highly infectious respiratory disease caused by Bordetella pertussis and is spread by respiratory droplets. The characteristic paroxysmal cough with inspiratory whoop seen among unvaccinated children is less common in individuals who have some acquired immunity from vaccination or infection.⁷⁵ Most deaths occur in unvaccinated infants under 6 months of age. Complications include pneumonia, atelectasis, seizures, encephalopathy, and hernias, with pneumonia as the most common cause of death.²¹

Epidemiological situation in 2013

In 2013, there were 12,341 notifications of pertussis. A 49% decrease in notified cases compared with 2012 (n=24,074) and 14% less than in 2008 (n=14,286) the year in which the most recent Australia-wide epidemic,⁷⁶ which peaked in 2011, began (Figure 58 and Figure 59). There were no pertussis related deaths reported in 2013.

Figure 58: Notified cases and notification rate for pertussis, Australia, 1993 to 2013, by year of diagnosis

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Figure 59: Notified cases of pertussis, Australia, 2008 to 2013, by month and year of diagnosis and state or territory

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Geographic description

In 2013, all jurisdictional specific rates decreased compared with 2012. Despite the timing of peak pertussis activity in the most recent epidemic period varying across jurisdictions, in 2013 most jurisdictional specific rates had returned to or were approaching, pre-epidemic levels. However, activity remained high in Tasmania (100 per 100,000) and Western Australia (65 per 100,000) compared with pre-epidemic rates in those states (Figure 60).

Age and sex distribution

Females accounted for 57% (n=6,986) of cases in 2013. Females had higher rates across all age groups, except among adults aged 80 years or over (Figure 61). The highest notification rate in both males and females occurred in the 5–9 years age group (117 and 130 per 100,000 respectively). Notification rates in females were on average 1.6 times that of males in the 25–64 years age groups.

Figure 60: Notification rate for pertussis, 2008 to 2013, by year of diagnosis and state and territory

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Figure 61: Notification rate for pertussis, Australia, 2013, by age group and sex

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In 2013, the trend prominent in this recent epidemic period of higher notification rates in children less than 15 years of age compared with those 15 years of age or over continued. Children less than 15 years of age represented 39% (n=4,807) of notifications and had a notification rate (110 per 100,000) 2.7 times higher compared with those 15 years of age or over (40 per 100,000). However, rates in children less than 15 years of age have declined steeply since reaching a peak in 2011. The highest age specific rates in 2013 occurred in the 5–9 years age group (123 per 100,000) consistent with the trend since 2010, while all age group rates continued the downward trend commenced in 2012 (Figure 62).

Figure 62: Notification rate for pertussis, Australia, 2008 to 2013, by year of diagnosis and selected age groups

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Vaccination

The NIP schedule in 2013 included a primary course of 3 doses of vaccine at 2, 4, and 6 months of age, with additional booster doses provided at 4 years of age and between 10 and 15 years of age.⁵⁰

Pertussis vaccine effectiveness among Australian children has been estimated to range from 82%–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 2003.⁷⁷ Immunity to disease decreases over time post-vaccination with estimates of protection remaining for 4–12 years.^78–80

In order to determine the vaccination status of cases, public health follow-up is required. During large epidemic periods the follow-up of all cases is not feasible and as per the pertussis national guidelines for public health units,⁸¹ jurisdictions prioritise case follow-up to those less than 5 years of age. During 2013, those aged less than 5 years accounted for 12% (n=1,458) of all notified cases and information about vaccination status was available for 93% (n=1,350) of these cases.

For children eligible to receive the full primary course of 3 vaccinations, 66% (n=664) had done so and 24% (n=49) of those eligible had received the full scheduled course of 4 doses (Table 15).

Table 15: Notified cases of pertussis in children aged 0 to 5 years, Australia, 2013, by age group and number of doses of vaccine

	Number of vaccine doses					Unknown	Total
Age group	0	1	2	3	4
Less than 6 weeks of age (not eligible for vaccination)	49	5				20	74
6 weeks to <4 months (eligible for 1 dose of vaccine)	22	72	6			7	107
4 to < 6 months (eligible for two doses of vaccine)	7	17	33			1	58
6 months to < 4 years (eligible for 3 doses of vaccine)	85	33	174	662	2	56	1,012
4 to 5 years (eligible for 4 doses of vaccine)	27	4	28	75	49	24	207
Total	190	131	241	737	51	108	1,458

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 receiving at least the 2nd vaccine dose at 4 months of age.⁸² Seventy-one per cent (n=1,029) of cases less than 5 years of age had received at least 2 doses of a pertussis-containing vaccine.

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Discussion

Epidemics of pertussis have historically occurred at regular intervals of approximately 4 years on a background of endemic circulation in Australia. The most recent epidemic appears to be over, with most jurisdictions reporting pertussis activity consistent with pre-epidemic levels. Notification rates have decreased in all states and territories and across all age groups in 2013 compared with their epidemic peaks. Most jurisdictions correspondingly ceased their respective cocooning programs in 2012, which included various combinations of providing free booster vaccinations to pregnant women, parents and carers of infants with only the Northern Territory and New South Wales continuing this strategy into 2013.

Poliomyelitis

• Australia was certified by the WHO in 2000 as having eradicated Indigenous poliovirus.
• There were no cases of poliomyelitis identified in Australia in 2013.

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; however in less than 1% of cases the virus may invade the nervous system and cause acute flaccid paralysis (AFP).²¹

Vaccines formulated with inactivated poliovirus, are available in combination with diphtheria toxin, tetanus and other antigens. The NIP schedule in 2013 recommended a primary course of 3 doses at 2, 4, and 6 months of age, with additional booster doses at 4 years and between 10 and 15 years, delivered through school based programs.⁵⁰

In 2013 there were no notifications of poliomyelitis. Australia, along with the Western Pacific Region, remains 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 free country is 1 case of AFP per 100,000 children less than 15 years of age. Australia has achieved this surveillance target in all years since 2008. However, the virological surveillance indicator of adequate stool specimen collection in 80% of AFP cases has never been met. More details can be found in the annual report series published in the CDI by the Australian Enterovirus Reference Laboratory who coordinate poliovirus surveillance activities in Australia.

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Rubella and congenital rubella syndrome

• Rubella is a rare disease in Australia.
• Since 2003, rubella notifications have been less than 0.3 per 100,000.
• In 2013 there were 25 cases of rubella and 2 cases of congenital rubella syndrome reported.

Rubella is generally a mild and self-limiting viral infectious disease. It is spread from person to person through contact with respiratory secretions, including aerosol transmission. Clinically, rubella can be difficult to distinguish from other diseases that also cause febrile rash, such as measles, and is asymptomatic in up to 50% of cases.²¹

Epidemiological situation in 2013

In 2013 there were 25 cases of rubella reported, which was a rate of 0.1 per 100,000. While this is consistent with the low rates of this disease experienced since 2003, it is a marked decline from the peak rate of more than 30 per 100,000 in 1995 (Figure 63). Indigenous status was recorded for all cases, none of which were reported as Indigenous. There were 2 cases of congenital rubella syndrome (CRS) reported in 2013. Both cases were imported, one each from Nepal and Thailand. The first was a newly arrived refugee infant born overseas and diagnosed later on arrival in Australia. The 2nd infant was born in Australia to a non-immune mother who acquired her infection whilst overseas.

Figure 63: Notification rate for rubella, Australia, 1991 to 2013, by year of diagnosis

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Geographic distribution

Cases were reported from New South Wales (n=12), Queensland (n=6), Victoria (n=3), South Australia (n=2) and one each from the Australian Capital Territory and Western Australia (Figure 64).

Figure 64: Notified cases of rubella, Australia, 2008 to 2013, by month and year of diagnosis and state or territory

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Age and sex distribution

There were approximately equal numbers of males (n=13) and females (n=12) in 2013. The median age was 29 years (range 8–85 years) (Figure 65). Consistent with previous years, the majority of cases (52%) occurred in adults aged 20–39 years of age. Of all female cases, 83% (n=10) were notified in women of child bearing age (15–44 years) (Figure 65).

Figure 65: Notification rate for rubella, Australia, 2013, by age group and sex

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When reviewing the age and sex trend since 1991, a change in the epidemiology is evident. Between 1991 and 2002, males represented 67% of all notifications. The highest age group rates during this period occurred in the male 15–19 years age group at 31 notifications per 100,000 (Figure 66). In contrast, between 2003 and 2013 the male to female rate ratio was roughly equal with males representing 54% of all notifications. During this later period the highest rates occurred at an older age occurring in the 25–29 years age group (0.3 per 100,000) (Figure 67). The median age also increased from 18 years of age between 1991 and 2002 to 29 years of age between 2003 and 2013.

Figure 66: Notification rate for rubella, Australia, 1991 to 2002, by age group and sex

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Figure 67: Notification rate for rubella, Australia, 2003 to 2013, by age group and sex

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Vaccination

Rubella vaccine is provided in the combined MMR or MMRV vaccine and in 2013 was provided under the NIP schedule at 12 months and 4 years of age. From 1 July 2013, the 2nd dose is recommended at 18 months of age.⁵⁰

The primary aim of immunisation against rubella is to prevent cases of CRS.⁸³ Two doses of a rubella containing vaccine are recommended for all non-immune persons born during or since 1966 and who are greater than 18 months of age.

Of the 25 cases notified in 2013, 72% (n=18) were of unknown vaccination status and a further 24% (n=6) were reported as unvaccinated. One case was vaccinated; an 8-year-old child who had received both doses of a rubella-containing vaccine. The high level of incompleteness in this field for rubella makes any additional analysis difficult.

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Discussion

The WHO Western Pacific Region, of which Australia is a member, has also endorsed accelerated rubella and CRS goals, and more recently proposed a regional goal of elimination with a target year yet to be determined.⁸⁴

Evidence suggests that endemic rubella is well controlled in Australia. A marked decline in rubella notifications since 2003 has seen rates consistently well below the 1 per 100,000 WHO goal indicative of rubella control.⁸⁵ The increasing trend in age of notifications likely reflects the declining rates of rubella among children since routine MMR immunisation was implemented and the subsequent achievement of high 2 dose coverage. Males, historically more susceptible because universal vaccination was not introduced until 1989, no longer appear to be at greater risk of infection compared with females.

Congenital rubella syndrome is rare in Australia and in recent years mainly occurs among infants of overseas-born women, a cohort previously identified as being at risk of non-immunity to rubella.

Improvements in surveillance data would include more routine genotyping of cases and increased completeness of vaccination status, particularly among high risk groups.

Tetanus

• Cases of tetanus are uncommon in Australia.
• Cases generally occur in older unvaccinated people or in those who have not received a booster dose in the last 10 years.
• In 2013, there were 4 cases of tetanus reported, with no notified deaths

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 manured soil.²¹ 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. The disease usually occurs after an incubation period of 3 to 21 days (ranging from 1 day to several months), with a median time of onset at 10 days post injury. In Australia, tetanus is rare, occurring primarily in older adults who have never been vaccinated or were vaccinated in the remote past. A high level of diagnostic awareness of tetanus is important in the elderly, as most deaths occur in people over 70 years of age, especially women, and may be associated with an apparent minor injury.⁵⁰

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Epidemiological situation in 2013

In 2013, there were 4 notifications of tetanus, which was consistent with the low numbers of this disease notified in recent years. The place of acquisition for 3 cases was reported as Australia (Figure 68). There were no reported deaths due to tetanus.

Figure 68: Notified cases of tetanus, Australia, 2002 to 2013, by year of diagnosis and state or territory

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Age and sex distribution

The 4 cases comprised 3 males and 1 female. One case was in the 30–34 years age group and the remaining 3 cases were over 60 years of age.

Indigenous status

Indigenous status was complete for 3 of the 4 cases, none of which were reported as Indigenous.

Vaccination

The NIP schedule in 2012 recommends a primary course of tetanus vaccination including 3 doses provided at 2, 4, and 6 months of age. Two booster doses are provided at 4 years and between 10 and 15 years delivered through school based programs. Booster doses are additionally recommended for all adults at the age of 50 years who have not received one in the previous 10 years. Complete immunisation induces protection lasting throughout childhood but by middle age 50% of vaccinees have low or undetectable levels of antibodies. However, tetanus is uncommon in people who have received 4 or more doses of a tetanus-containing vaccine and in those who received their last dose within 10 years.⁵⁰

Of the 4 cases in 2013, one had received a single dose of a tetanus-containing vaccine and the remaining 3 cases, all of whom were over 60 years of age, were either not vaccinated or reported with an unknown vaccination status.

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Varicella zoster virus

• In 2013, a total of 16,986 cases of varicella zoster virus infection were reported, which was an increase of 14% from 2012.
• 58% of cases were reported as unspecified varicella zoster infection, 30% of cases were reported as shingles and 12% of cases were reported as chickenpox.

The varicella zoster virus (VZV) is a highly contagious member of the herpesvirus family and causes 2 distinct illnesses; chickenpox as the primary infection; and following initial infection, shingles (herpes zoster), which occurs following reactivation, often many years later, of latent virus in approximately 20% to 30% of cases of chickenpox overall. Shingles occurs more frequently among older adults (most commonly after 50 years of age) and in immunocompromised people.²¹

In 2006, CDNA agreed to make the 3 categories of VZV infection nationally notifiable; ‘chickenpox’, ‘shingles’ and ‘varicella zoster virus unspecified’. By 2009 all jurisdictions were notifying VZV infections to the NNDSS with the exception of New South Wales, where VZV is not notifiable.

The ability to categorise a VZV infection as chickenpox or shingles depends largely on clinical evidence. Due to the absence of information on clinical presentation for many cases, the majority of VZV infections nationally are reported as unspecified.

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Epidemiological situation in 2013

In 2013, there were 16,986 VZV notifications from the 7 reporting jurisdictions. This was a 14% increase on cases notified in 2012 (n=14,898). Of the total VZV notifications in 2013, 58% (n=9,927) of cases were reported as unspecified varicella infection, 30% (n=5,071) as shingles and 12% (n=2,042) as chickenpox (Figure 69 and Figure 70).

Figure 69: Notified cases of varicella zoster virus infection, 2013, by age group*

* Excluding New South Wales.

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Figure 70: Proportion of notified cases of varicella zoster virus unspecified, chickenpox and shingles, 2013, by state or territory*

* Excluding New South Wales.

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Varicella zoster virus (unspecified)

• Notifications of varicella zoster virus infection (unspecified) are laboratory confirmed cases that are positive for varicella zoster virus, that do not have the clinical diagnosis available to distinguish as chickenpox or shingles.
• In 2013 there were 9,927 cases of varicella zoster virus (unspecified) reported, which was an increase of 18% from 2012.

Epidemiological situation in 2013

In 2013, there were 9,927 cases of unspecified VZV infections reported. This represented a notification rate of 63 per 100,000 and an 18% increase in notifications compared with 2012 (n=8,437).

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Geographic description

The highest notification rate for unspecified VZV was reported from Queensland at 115 per 100,000 (n=5,337) followed by Victoria at 53 per 100,000 (n=3,018) and Western Australia at 49 per 100,000 (n=1,230). VZV unspecified rates should be interpreted with caution as they are dependent on the individual jurisdictional practice of following up laboratory notifications to establish clinical presentation. For example, Queensland routinely conducts follow-up for cases of VZV in those under 8 years of age, leading to a high proportion of VZV infections in older age groups classified as unspecified.

Age and sex distribution

The male to female ratio in the unspecified VZV notifications was 0.8:1. Females have an overall higher notification rate (69 cases per 100,000) compared with males (57 per 100,000), which predominates across the majority of age groups. The highest age group specific notification rates occurred in the 85 years or over age group for females, (133 per 100,000) and in the 75–79 years age group for males, (124 per 100,000). The lowest age group specific notification rates were in the 0–4 years age group for both males and females. These age distribution trends are likely reflect the practice of increased follow-up among younger age groups, especially in children aged less than 15 years, to determine clinical presentation (Figure 71).

Figure 71: Notification rate for varicella zoster virus unspecified, Australia,* 2013, by age group and sex

* Excluding New South Wales.

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Chickenpox

• Chickenpox is normally a mild disease that occurs in childhood. However, in about 1% of cases complications can arise.
• The primary purpose of the vaccine is to prevent deaths, reduce the severity of disease and in the longer term reduce rates of VZV reactivation as shingles.
• In 2013, there were 2,042 cases of chickenpox reported, a 3% increase from 2012 (n=1,977).

Chickenpox is a highly contagious infection spread by respiratory secretions, including aerosol transmission, or from the vesicle fluid of skin lesions from 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 persons of any age who are immunocompromised, in whom complications, disseminated disease, and fatal illness are more likely to occur.⁵⁰

Epidemiological situation in 2013

In 2013, there were 2,042 cases of chickenpox reported. Representing a notification rate of 13 per 100,000 and a 3% increase in the number of notifications compared with 2012 (n=1,977). Rates of chickenpox have remained stable between 12 and 14 per 100,000 in all years since 2009.

Geographic description

The highest notification rate, 40 per 100,000, was reported from the Northern Territory (n=97), followed by South Australia, 23 per 100,000 (n=386), reflecting the increased case ascertainment in these jurisdictions compared with others.

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Age and sex distribution

The male to female ratio in 2013 was 1.1:1 with 1,065 notifications for males and 968 for females. Seventy-four per cent of notified chickenpox cases (n=1,501) occurred in children less than 10 years of age. The 5–9 years age group had the highest notification rate for both sexes, (80 per 100,000 for males and 69 per 100,000 for females) (Figure 72). Although higher rates among children compared with adults is expected for chickenpox, the distribution of cases by age group also reflects general jurisdictional practice of limiting follow-up for cases in children less than 15 years of age.

Figure 72: Notification rate for chickenpox, Australia,* 2013, by age group and sex

* Excluding New South Wales.

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Vaccination

Routine use of a varicella-containing vaccine in children was first recommended in Australia in 2003. In November 2005, the vaccine was funded under the NIP for all children at 18 months of age, with a school-based catch-up program for children 10–13 years of age with no history of disease or previous vaccination.

In 2013, the oldest cohort of children eligible for varicella vaccination at 18 months of age under the NIP would be 9 years of age. The analysis of vaccination status is restricted to this cohort. Vaccination status information was available for 50% (n=504) of cases that occurred in children less than 10 years of age who were eligible for vaccination with 76% (n=381) vaccinated and 24% not vaccinated (n=123). Post-marketing studies in the United States of America have estimated the effectiveness of 1 dose of monovalent varicella vaccine in children to be 80%–85% against any disease and 95%–98% against severe varicella.⁸⁶

Shingles

• Herpes zoster or shingles is a sporadic disease caused by reactivation of latent varicella zoster virus following primary infection of chickenpox.
• In 2013, there were 5,017 cases of shingles reported, which was a 12% increase from 2012.

Shingles occurs most commonly with increasing age, impaired immunity, and a history of chickenpox in the 1st year of life.⁵⁰ Reactivation of VZV to cause shingles is thought to be due to a decline in cellular immunity to the virus. Shingles typically presents as a unilateral vesicular rash localised 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 however, complications develop in approximately 30% of cases, the most common of which is chronic severe neuropathic pain or post herpetic neuralgia.²¹

A single dose of zoster vaccine is recommended, but not presently funded through the NIP, for adults aged 60 years or over who have not previously received a dose of zoster vaccine.⁵⁰

Epidemiological situation in 2013

In 2013, there were 5,017 cases of shingles reported to the NNDSS. This was a notification rate of 32 per 100,000 and an 11% increase compared with 2012 (n=4,507).

Geographic description

The highest rates of shingles occurred in South Australia with 114 per 100,000 (n=1,899), followed by the Northern Territory, 102 per 100,000 (n=246). The high rates in these jurisdictions most likely reflect their higher levels of case ascertainment compared with other jurisdictions.

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Age and sex distribution

The notification rate was lower in males at 29 per 100,000 compared with females at 35 per 100,000, representing a ratio of 0.8:1.

As expected, rates increased with age with the highest in the 80–84 years age group for males, 87 per 100,000 and in the 85 years or over age group for females, 93 per 100,000 (Figure 73).

Figure 73: Notification rate for shingles, Australia,* 2013, by age group and sex

* Excluding New South Wales.

Text version of Figure 73 (TXT 1 KB)

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Discussion

Rates of chickenpox have remained relatively stable in all years since 2009. Noting that 2009 was the 1st year in which all jurisdictions, with the exception of New South Wales, reported cases to the NNDSS. An unpublished analysis of these data show an increase in shingles notifications in South Australia since 2006, which is consistent with an upward trend noted in the national data since 2009. This increase is likely to be due to multiple factors including changes in health-care seeking behaviour, clinical practice, and awareness of reporting requirements as well as an ageing population.

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