Results -continued

Vaccine preventable diseases

Surveillance objectives

This section summarises the national surveillance data for notifiable diseases targeted by the National Immunisation Programme (NIP) in 2012. These include diphtheria, invasive Haemophilus influenzae (Hib) type b infection, laboratory confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease (IPD), 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, are reported under bloodborne diseases and other bacterial infections, respectively. Other vaccine preventable diseases (VPDs) presented 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, have been published in the regular CDI Vaccine Preventable Diseases in Australia supplements.⁴⁵ The more recent Australian vaccine preventable diseases epidemiological review series published in CDI, contain additional analysis on individual diseases.^46–49

In 2012, there were 85,810 notifications of VPDs reported to the NNDSS, representing 35% of all notifications and a 5% increase compared with 2011 (81,872 cases) (Table 3). Influenza was the most commonly notified VPD with 44,563 (52%) cases reported, followed by pertussis (24,069 cases, 28%). The number of notifications and notification rates for VPDs in Australia are shown in Tables 4 and 5.

Vaccination coverage

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. Nonetheless, vaccination substantially lowers the chance of becoming infected and/or reduces 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 a field capturing the number of doses. In January 2008 new, more detailed fields were incorporated for recording vaccine type, vaccination validation 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 2012, 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 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 Handbook²⁰ 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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Diphtheria

Diphtheria is an acute toxin-mediated systemic disease caused by the toxigenic strains of 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 direct contact with skin lesions, or articles soiled by infected individuals.¹⁶ Non-toxigenic strains of C. diphtheriae usually only cause mild throat or skin infection and are not nationally notifiable.¹⁹

The NIP schedule in 2012 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.²⁰

In 2012, there were no notifications of diphtheria reported to the NNDSS. Whilst diphtheria is now rare in Australia, in 2011 there were 4 cases reported and prior to this, 1 case of cutaneous diphtheria reported in 2001. All these cases were associated with imported infections from countries where diphtheria remains endemic.

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Influenza

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.⁵⁰ The disease caused by infection with influenza viruses ranges from asymptomatic⁵¹ through 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.⁵² The goals of influenza surveillance are to determine the severity, intensity and distribution of illness, detect outbreaks, monitor for changes in the virus and to facilitate policy development and planning.⁵³

Vaccination

Seasonal influenza vaccination is the primary means of preventing influenza and its complications and is included in the NIP for specific groups of the population. In 2012, the NIP funded influenza vaccine for people aged 6 months or over with medical conditions placing them at risk of severe disease. It was also included for Aboriginal and Torres Strait Islander people aged 15 years or over, pregnant women and those aged 65 years or over.

Epidemiological situation in 2012

In 2012, there were 44,563 notifications of laboratory confirmed influenza. This was almost twice the number of notified cases reported the previous year and a more than 3-fold increase from 2010. Notification rates were highest in South Australia (380 per 100,000) and Queensland (369 per 100,000). Notifications in Western Australia, Tasmania, the Northern Territory and the Australian Capital Territory were similar to the national notification rate of 196 per 100,000, while the Victorian notification rate was substantially lower than the national notification rate at 106 per 100,000. Queensland reported the highest number of influenza cases of any jurisdiction, comprising 38% of all notifications, which was consistent with previous years with the exception of 2010 (Figure 33).

Figure 33: Notifications of laboratory confirmed influenza, Australia, 2012, 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 age group, accounting for 26% of all notifications (Figure 34). Notification rates were highest in the 0–4 years and 85 years or over age groups (454 and 380 per 100,000 respectively) (Figure 34). The overall age distribution was characteristic of previous A(H3N2)-dominated seasons where preschool-age children and older adults were particularly affected (Figure 34).⁵⁴

Figure 34: Notifications of laboratory confirmed influenza, Australia, 2012, by age group and sex*

* Excludes 224 notifications for which age and/or sex were not reported.

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In 2012, females accounted for 23,890 (54%) of the influenza notifications for which sex was reported. Notification rates per 100,000 were higher among females in the 15–74 years age groups whereas males dominated the younger (0–14 years) and older (over 75 years) age groups (Figure 35).

Figure 35: Notification rate for laboratory confirmed influenza, Australia, 2008 to 2012, by age group and year

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Seasonality

Influenza activity during the 2011–2012 inter-seasonal period was the 2nd highest on record behind that observed in 2010–2011. Excluding 2009, notifications of influenza in 2012 started their seasonal increase earlier, rose sharply and peaked higher compared with previous years. Activity in the majority of jurisdictions peaked around mid-July. However, ongoing increased activity continued to be reported in Queensland, which peaked in mid-August and South Australia, which had a distinct second peak in late November (Figure 36).

Figure 36: Notifications of laboratory confirmed influenza, Australia,* 2007 to 2012, by month and year

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

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Mortality

Nationally, there were 85 influenza-associated deaths notified to the NNDSS, with a median age of 80 years (range < 1–102). Approximately 88% (n=81) of those who died were reported as having influenza A (unsubtyped) or A(H3N2). Indigenous status was reported for 69% (n=67) of influenza-associated deaths notifications; Aboriginal and Torres Strait Islander peoples accounted for 9% (n=6) of influenza-associated deaths notifications. 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.

Virological surveillance

In 2012, typing data were reported for all but 4 laboratory-confirmed influenza notifications. Of the notifications with typing information, 76% were type A, (59% A (unsubtyped), 16% A(H3N2) and <1% A(H1N1)pdm09) and 24% were type B. Mixed influenza type A and B infections, and influenza type C together accounted for <1% of notifications (Figure 37). The ratio of influenza A to B was similar in 2011 and 2012. However, the distribution of A subtypes was markedly different, with 2012 being the first year since the 2009 pandemic not dominated by the H1N1 pandemic strain.

Figure 37: Notifications of laboratory confirmed influenza,* Australia, 2012, by week and subtype

* Excludes 81 mixed type A and B, type C and untyped influenza infections.

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For 2012, the WHO Collaborating Centre for Reference and Research on Influenza (WHOCC) analysed 2,226 specimens from Australian influenza cases. This represented approximately 5% of the 44,563 laboratory confirmed cases reported to the NNDSS. Influenza A(H3N2) comprised 61% (n=1,357) of influenza viruses followed by influenza B ( 35% n=788) and influenza A(H1N1)pdm09 3.6% (n=81) (Figure 38).

Figure 38: WHO Collaborating Centre for Reference and Research on Influenza subtyped influenza virus samples, Australia, 2011 and 2012

A

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B

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The WHOCC assessed the antigenic similarity of circulating influenza virus isolates to reference strains by haemagglutination inhibition (HI) (n=1,742 influenza virus isolates). The majority of A(H3N2) isolates (1,115 of 1,118) were characterised as A/Victoria/361/2011-like, while the remainder were A/Perth/16/2009-like. No ‘low reactor’ A(H3N2) isolates were identified. All of the A(H1N1) viruses circulating (n=38), were antigenically similar to A/California/7/2009-like virus with 24% (n=9) characterised as ‘low reactors’. Many of the low reactors had changes in the 153–158 amino acid region of the haemagglutinin (HA) gene, which have been shown to reduce reactivity in HI assays. Comparison of HA genes from the original clinical samples suggest that the mutations are artefacts caused by isolation in Madin Darby canine kidney (MDCK) cells or in eggs.⁵⁵ Similarly, 90% (n=528) of influenza B viruses were closely related to the B/Brisbane/60/2008-like (B/Victoria lineage) virus with 25% (n=131) characterised as ‘low reactors’. The remaining 10% (n=58) of influenza B viruses were characterised as B/Wisconsin/1/2010-like, which belong to the B/Yamagata lineage. Except for the A(H3N2) viruses, the majority of influenza type A(H1N1) and B viruses that circulated during 2012, were antigenically similar to the 2010, 2011 and 2012 vaccine viruses.

Viruses collected in 2012 were also tested for sensitivity to the neuraminidase inhibitor class of antiviral drugs. A neuraminidase inhibition assay was performed on 1,715 virus isolates consisting of 1,126 A(H3N2), 43 A(H1N1)pdm09 and 546 B viruses. Resistance to oseltamivir was detected in a single A(H1N1)pdm09 isolate and was mediated by the well characterised H275Y mutation. All influenza B isolates examined were sensitive to oseltamivir. Further, all isolates were sensitive to zanamivir.

Additional surveillance activities

In addition to NNDSS data, a series of targeted influenza surveillance systems operated during 2012. 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 sources of data:

Discussion

The 2012 influenza season in Australia began in May, peaked in mid-July and was largely concluded by the end of September. Australia experienced sustained virus circulation until late August, particularly in Queensland before steadily decreasing. Peak NNDSS notifications in 2012 occurred approximately 5 weeks earlier than the median week of peak transmission for the period of 2003 through 2011.⁵⁶ The most commonly detected virus was influenza A(H3N2), however influenza type B was a significant virus later in the year and was almost wholly responsible for South Australia’s second wave of infections. The resurgence of A(H3N2) in Australia was associated with a shift in the age distribution of disease, compared with recent years when A(H1N1)pdm09 was the predominant virus circulating. The dominance of A(H3N2) coincided with a return to the more typical seasonal influenza pattern where the elderly and young infants are disproportionately affected.

Taken together, data from most influenza surveillance systems showed that the overall impact of influenza in 2012 was somewhat greater than average. At the seasonal peak, the number of influenza notifications reported per week and ILI consultation rates were higher than in any previous season since 2007, except for the 2009 pandemic.^57,58 In the New South Wales Registered Death Certificates data, the rate of deaths classified as influenza and pneumonia met or exceeded the epidemic threshold for most of July, which was higher than in the previous 2 years, but lower than in 2007 and 2008.⁵⁹

In summary, notifications of influenza in 2012 started their seasonal increase earlier, rose sharply and peaked higher and for longer in comparison with previous years. When NNDSS notification data are combined with companion influenza surveillance systems, notification data supports the observation that 2012 was the most severe season since the beginning of notification in NNDSS, with the exception of 2009.

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Invasive Haemophilus influenzae type b disease

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).

In 2012, the NIP schedule included 3 doses of a conjugate Hib vaccine at 2, 4 and 6 months of age, followed by a booster dose at 12 months of age.²⁰

Epidemiological situation in 2012

In 2012, there were 15 notifications of Hib disease. This was similar to the number of cases reported in 2011 (n=13), and less than the mean of the previous 5 years (n=20). The 2012 notification rate was 0.07 per 100,000 and was consistent with the very low rates that have been seen since the introduction of the vaccine on the NIP in July 1993 (Figure 39). Cases occurred in all jurisdictions, except the Australian Capital Territory and the Northern Territory. The notification rates vary widely because of the low overall number of notifications. There were 2 deaths reported in 2012, one in a partially vaccinated infant and one in an unvaccinated adult over 60 years of age.

Figure 39: Notifications and notification rates for invasive Haemophilus influenzae type b infection, Australia, 1992 to 2012, by year of diagnosis

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Age and sex distribution

In 2012, the male to female ratio was 1.5:1. One-third of cases (n=5) were in children aged less than 5 years and 60% of these were among infants aged less than 1 year of age. The 0–4 years age group also had the highest notification rate (0.34 per 100,000). The remaining cases were among adults, ranging in age from 45–84 years (Figure 40).

Figure 40: Notification rate for invasive Haemophilus influenzae type b infection, Australia, 2012, by age group and sex

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Indigenous status

Indigenous status was 100% complete in 2012. Two cases were reported as being Indigenous in 2012; a notification rate of 0.34 per 100,000. This rate was consistent with 2011, but much lower than 2010 (1.42 per 100,000). High routine Hib vaccination coverage has been achieved in Indigenous populations.²⁰

Vaccination status

In 2012, persons aged less than 20 years had been eligible for Hib vaccination through the NIP during infancy, following addition of the vaccine to the NIP in 1993. Eight of the 15 Hib notified cases reported in 2012 were aged less than 20 years. Of these cases, five were aged over 12 months and eligible for the full vaccine course, of which 2 cases were fully vaccinated, two were not vaccinated and one was partially vaccinated. The remaining 3 cases were aged less than 12 months and although they were fully vaccinated for their age, they had not yet completed the full course.

Discussion

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 (Figure 39). Australia now has one of the lowest rates of this disease in the world.⁴⁵

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Invasive pneumococcal disease

IPD is a disease in which Streptococcus pneumoniae is isolated from a normally sterile site such as blood, cerebrospinal fluid or pleural fluid. 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 sometimes coma. S. pneumoniae is part of the normal bacterial flora in the throat and nose of infants and young children, where it does not cause disease. The bacterium is spread to people in close proximity through inhalation of respiratory droplets containing live bacteria that are produced when an infected person coughs or sneezes.

Epidemiological situation in 2012

There were 1,822 notifications of IPD reported in 2012, representing a rate of 8.0 per 100,000 Compared with 2011, the national number of IPD notifications in 2012 decreased by 3.3% but was the 2nd highest reported in any year since the introduction of the universal pneumococcal conjugate vaccine program for young children in 2005 (Figure 41). The notification rate for IPD varied from 6.8 per 100,000 in Victoria to 30.6 per 100,000 in the Northern Territory.

Figure 41: Notifications of invasive pneumococcal disease, Australia, 2012, by month of diagnosis and age group

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The number of notifications in New South Wales and Queensland increased while they remained constant in the Australian Capital Territory, and all other jurisdictions reported fewer notifications. The largest change in IPD notification rates was in the Northern Territory where the rate (31 per 100,000) declined to levels similar to that seen prior to the 2011 serotype 1 outbreak (56 per 100,000).⁶⁰ The increase in notifications from Queensland, which commenced in 2011, continued with 348 notifications reported in 2012. Further, notifications in New South Wales increased by 9% from 529 notifications in 2011 to 579 in 2012.

Seasonality

Many respiratory diseases including IPD, are known to show distinct seasonality peaking during the winter months). The number of IPD cases in 2012 was greatest in the winter months, with the peak in August (n=270) (Figure 41).

Age and sex distribution

The age-specific notification rate for IPD in 2012 was trimodal, with the highest rates being in young children under the age of 5 years and older Australians (60 years or over) with a smaller peak in the 35–44 years age group (Figure 42).⁶¹ In older Australians, the highest notification rate was in those aged 85 years or over (39 per 100,000) while the highest rate in children aged less than 5 years was in those aged 1 year (18 per 100,000). In 2012, males accounted for 51% of all cases of IPD (Figure 42).

Figure 42: Notification rate for invasive pneumococcal disease, Australia, 2012, by age group and sex

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Indigenous status

Completeness of Indigenous status reporting in 2012 was high, with 86% (n=1,564) of cases having known Indigenous status, of which 16% were reported as being Indigenous (n=244). In 2012, the notification rate for IPD in the Indigenous population (41 per 100,000) was almost 7 times that for non-Indigenous people (6 per 100,000). In 2012, the notification rate for IPD among Indigenous children aged less than 5 years (37.1 cases per 100,000) remained almost 3-fold that of the general population (10.5 per 100,000) (Figure 43).

Figure 43: Notification rate for invasive pneumococcal disease, Australia, 2002 to 2012, by Indigenous status 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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Vaccination

There are 4 pneumococcal vaccines available in Australia, each targeting multiple serotypes (Table 17). In Australia, pneumococcal vaccination is included on the NIP schedule and recommended for all infants, Australians aged 65 years or over, Aboriginal and Torres Strait Islander peoples aged 50 years or over and the medically at-risk.²⁰

Table 17: Streptococcus pneumoniae serotypes targeted by pneumococcal vaccines

Vaccine type	Serotypes targeted by the vaccine
7-valent pneumococcal conjugate vaccine (7vPCV)	4, 6B, 9V, 14, 18C, 19F and 23F
10-valent pneumococcal conjugate vaccine (10vPCV)	1, 4, 5, 6B, 7F, 9V, 14, 18C, 19F and 23F
13-valent pneumococcal conjugate vaccine (13vPCV)	1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F
23-valent pneumococcal polysaccharide vaccine (23vPPV)	1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19F, 19A, 20, 22F, 23F and 33F

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There were several amendments to the NIP schedule in 2011 and 2012 with the most notable being the July 2011 replacement of the 7-valent pneumococcal conjugate vaccine (7vPCV) and the 10-valent pneumococcal conjugate vaccine (10vPCV) for all infants with the 13-valent pneumococcal conjugate vaccine (13vPCV) (Table 18).

Table 18: Amendments to the National Immunisation Program pneumococcal vaccination schedule for 2011 and 2012

Vaccine type	National Immunisation Program pneumococcal vaccination schedule
7-valent pneumococcal conjugate vaccine (7vPCV)	From 2005 to July 2011, 7vPCV was funded nationally for all infants as a 3-dose primary vaccination schedule consisting of doses at 2, 4 and 6 months of age without a booster in the 2nd year of life.
10-valent pneumococcal conjugate vaccine (10vPCV)	From October 2009 to September 2011, 10vPCV replaced the use of the 7vPCV in all children aged <2 years in the Northern Territory.
13-valent pneumococcal conjugate vaccine (13vPCV)	From July 2011, the 13vPCV replaced the 7vPCV for all infants. From October 2011, the 13vPCV replaced the 10vPCV for infants in the Northern Territory. From October 2011 to September 2012, a single supplementary dose of 13vPCV for children aged 12–35 months who completed primary vaccination with either 7vPCV or 10vPCV was made available for 12 months. From October 2012, a booster dose of 13vPCV was made available for Aboriginal and Torres Strait Islander children at 12–18 months of age.
23-valent pneumococcal polysaccharide vaccine (23vPPV)	From October 2011, the 23vPPV booster dose for Aboriginal and Torres Strait Islander children aged 18–24 months living in the Northern Territory, South Australia, Queensland and Western Australia ceased.

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More information on the current pneumococcal vaccination schedule in Australia can be found on the Immunise Australia web site (www.immunise.health.gov.au) and a detailed history of pneumococcal vaccination practices is available through the National Centre for Immunisation Research and Surveillance.⁶²

Serotype

Data on S. pneumoniae serotypes is important for understanding the effectiveness of vaccination programs. IPD serotypes were reported for 93% (n=1,690) of notified cases in 2012. The marked reduction in IPD due to serotypes targeted by the 7vPCV vaccine, seen in both Indigenous and non-Indigenous children aged less than 5 years has continued in 2012 (Figure 44). The 7vPCV serotypes accounted for only 6% (n=10) of IPD notifications where the serotype was known for children aged less than 5 years in 2012.

Figure 44: Notification rate of invasive pneumococcal disease in children aged less than 5 years, Australia, 2002 to 2012, by Indigenous status 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 vaccine replaced the 7vPCV component in the universal childhood immunisation program.

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From 2008 to 2011, there was an increase in the incidence of IPD due to the 6 additional serotypes targeted by the 13vPCV (13v-non-7v) vaccine in children under 5 years of age. This indicates that the serotypes of circulating S. pneumoniae had been replaced. In 2012, and following the July 2011 introduction of 13vPPV to the NIP, this trend was reversed with 13v-non-7v serotypes accounting for only 48% (n= 82) of IPD notifications compared with 68% (n=182) in 2011. For Aboriginal and Torres Strait Islander children, the most common 13v-non-7v serotype causing disease was due to serotype 1 (45% of 13v-non-7v serotypes), while in non-Indigenous children serotype 19A was the most common serotype reported (62%).

More detailed analyses of notification data can be found in the IPD annual reports published in CDI.⁶³

Measles

Measles is a highly infectious, acute viral illness spread by respiratory secretions, including aerosol transmission.⁶⁴ The incubation period is usually 10–14 days and it is infectious from around 4 days before and 4 days after the appearance of a characteristic rash. Initial symptoms last 2–4 days and are characterised by fever and malaise, followed by a cough, coryza and conjunctivitis. This is usually followed by a red blotchy rash, which typically begins on the face and then becomes generalised. Measles may be a severe disease with complications, which are more common in the chronically ill, children under 5 years of age and in adults over 20 years of age. Symptoms include otitis media, pneumonia, diarrhoea and acute encephalitis.^65,66 Subacute sclerosing panencephalitis is a late, rare (approximately 1 in 100,000 cases) manifestation of measles caused by persistent infection and is always fatal.²⁰

In 2012, measles vaccine was available in the combined measles-mumps-rubella (MMR) vaccine and provided under the NIP schedule to children at 12 months and 4 years of age. Two doses of a measles containing vaccine are recommended for all non-immune persons born during or since 1966 and who are 18 months of age or over. The MMR vaccine induces long term immunity to measles virus in 95% of recipients after a single dose and 99% of recipients after the 2nd dose.²⁰

Epidemiological situation in 2012

In 2012, there were 199 notifications of measles. This represents a notification rate of 0.90 per 100,000, which is 2.2 times the mean of the previous 5 years. The number of cases in 2012 was similar to that in 2011 when 193 cases were reported (Figure 45).

Figure 45: Notifications and notification rate for measles, Australia, 1997 to 2012, by year of diagnosis

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Geographical distribution

In 2012, cases of measles occurred in all states and territories, except the Australian Capital Territory and Tasmania (Table 4). The majority of these and the largest increase compared with 2011, occurred in New South Wales (n=170) (Figure 46). Over 86% of cases were associated with a large outbreak that occurred in Western and South Western Sydney and was linked to an imported case from Thailand.

Seasonality

In Australia, a seasonal pattern is no longer evident as the virus is not endemic (Figure 46). In temperate climates where measles transmission remains endemic, the majority of cases occur in late winter to early spring.¹⁹

Figure 46: Notifications of measles, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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Age and sex distribution

The male to female ratio was 1.1:1 in 2012, however there was a wide variation in this ratio across the age groups (Figure 47).

Figure 47: Notification rate for measles, Australia, 2012, by age group and sex

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In 2012, the age of measles cases ranged from 0–61 years with a median age of 15 years. Whilst notification rates increased across all age groups compared with previous years there were a higher proportion of cases aged less than 10 years of age (Figure 48). The highest age specific rates occurred in the less than 1 year age group at 13 per 100,000 (n=39), with rates also high in the 1–4 years and 10–19 years age groups (1.8 per 100,000 in each).

Figure 48: Notification rate for measles, Australia, 2007 to 2012, by age group

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The notification rates for measles remained below 2.5 per 100,000 for all age groups from 2007 to 2012. The exception to this was the under 1 year age group in 2011 and 2012 (Figure 48).

There were 39 cases aged less than 1 year and therefore too young to have received measles vaccine. The majority of these cases (92%) were aged between 6 and 12 months highlighting the loss of maternal antibody.⁶⁷

Indigenous status

Indigenous status was reported for 98% of cases during 2012 (n=194). Of these 6% (n=12) were reported as being Indigenous. All of these were reported from New South Wales, where Indigenous Australians had a notification rate 3 times higher than non-Indigenous people in that state (6.96 compared with 2.22 per 100,000 respectively).⁶⁸

Vaccination status

Of the 199 cases notified in 2012, 78% (n=155) were born after 1967 (or 1969 for New South Wales) and were over 12 months of age. This cohort was eligible for at least 1 dose of a publicly funded measles vaccine either during childhood or as a result of later measles vaccination catch up campaigns. Over 80% of vaccine eligible cases were either not vaccinated (43%, n=68) or of unknown vaccination status (42%, n=65). Of the remaining 15% (n=24) who were vaccinated, only three had received the full course of 2 doses of a measles vaccine (Figure 49).

Figure 49: Notifications of measles, Australia, 2012, by age group and vaccination status

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A high proportion of unvaccinated cases (48%, n=21) occurred in adolescents in the 10–19 years age group or young adults 20–29 years of age. Twenty-five cases occurred in those born between 1978 and 1982 (30–34 years age group) of which three were reported as receiving 1 dose of vaccine and the remainder were either not vaccinated (n=7) or were of unknown vaccination status (n=15). This cohort has previously been identified as being susceptible to measles virus infection as the second childhood measles vaccine now recommended at 18 months was not available to them and they were not targeted as part of the 1998 Measles Control Campaign.⁶⁹ In 2012, three of the cases were born before 1966, a cohort considered to have high levels of natural immunity. All three of these cases were either unvaccinated or of unknown vaccination status (Figure 49).⁷⁰

Source of infection and outbreaks

All but 1 case in 2012 were imported (10%, n=21) or linked to an imported case (89%, n=177). For the locally acquired case an epidemiological or virological link to an imported case could not be established (Figure 50).

Figure 50: Notifications of measles, Australia, 2012, by week of onset and source of infection

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Imported cases were either from the WHO South East Asia Region (81%), the majority of which were from Thailand (n=12) or the WHO Eastern Mediterranean Region (10%). A single case was reported from Uganda.

There were 6 clusters of two or more epidemiologically linked cases in 2012, all of which were import-related. In all except 1 cluster, transmission was interrupted quickly resulting in only 2 cases for each of these clusters. The largest outbreak of measles occurred predominately in Western and South Western Sydney. The outbreak comprised 173 cases in total, including 2 associated cases in the Northern Territory and three in South Australia. This outbreak began in April 2012 with an imported case from Thailand and peaked in September, with the last case reporting onset of symptoms on 29 November 2012. This outbreak included 24 generations of spread, lasting 33 weeks between the onset of symptoms of the first and last cases. NNDSS data indicate that of the 173 cases, 59% (n=102) were not vaccinated, 15% (n=26) had received 1 dose of a measles containing vaccine and 2 cases had received 2 doses, with the remaining cases being of unknown vaccination status. The median age of outbreak cases was 14 years of age (range 0–61 years).

Although there were several separate chains of transmission identified during the outbreak, all cases in each of the geographic areas in New South Wales had direct epidemiological links to the larger outbreak. In addition, there were no new importations identified during the outbreak period and the genetic sequences of measles virus isolates from cases in these clusters were identical, thus establishing the link to the larger outbreak.

Genotype

Genotyping data were available for all 6 clusters, accounting for 92% (n=183) of cases in 2012. Genotypes B3D8 and D9 were identified among the clusters across Australia (Figure 51). The largely New South Wales based outbreak was due to measles virus genotype D8.

Figure 51: Measles clusters, Australia, 2012, by state or territory, genotype and source of infection

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Discussion

The fluctuating nature of measles rates over time can be attributed to sporadic imported cases that occasionally result in clusters of locally acquired infection among susceptible contacts.

Evidence suggests that endemic measles was eliminated from Australia in 2005 and possibly earlier.⁷¹ Based on the WHO definition, Australia has continued to maintain this status over time. In 2012, none of the outbreaks persisted for more than 12 months with the longest lasting 33 weeks. Additionally, there was no evidence that a single genotype was continuously circulating for 12 months or more. Ongoing evidence of high population immunity was demonstrated by the rapid cessation of the majority of the outbreaks. Only one of the outbreaks in 2012 involved more than 3 generations of transmission, with there being 5–7 weeks between the onset of disease in the first case and the last cases.⁷² With the exception of the single case for which the source of infection could not be established, all of the 2012 cases were associated with an index case that was imported from overseas.

Mumps

Mumps is an acute viral illness with an incubation period of 12–25 days. Transmission is via 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%–70% of clinical cases; however a high proportion have non-specific symptoms including fever, headache, malaise, myalgia and anorexia.⁷³ Mumps encephalitis has been estimated to occur in 1 to 2 per 10,000 cases, with a case a fatality rate of around 1%.

In 2012, mumps vaccine was included in the combined MMR and provided under the NIP schedule at 12 months and 4 years of age. Two doses of a mumps containing vaccine are recommended for all non-immune persons born during or since 1966 and who are 18 months of age or over.

The mumps vaccine was first funded on the NIP schedule for infants of 12 months of age in 1982. Those born since that time are eligible for 2 doses of a mumps vaccine.⁷⁴

Epidemiological situation in 2012

In 2012, there were 200 notifications of mumps; a notification rate of 0.88 per 100,000. This represents a 28% increase compared with the 156 cases reported in 2011. Since 2009, mumps notifications have declined (Figure 52).

Figure 52: Notifications of mumps, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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Geographical distribution

Notifications were received from all states and territories except the Northern Territory. Notification rates were highest in the Australian Capital Territory (1.6 per 100,000) followed by New South Wales (1.4 per 100,000).

Age and sex distribution

In 2012, the male to female ratio was 1.3:1 with some variation between age groups. The highest rates for both males and females occurred in the 30–34 years age group at 3.5 and 2.4 per 100,000 respectively. The male specific rates were highest in the 25–39 years age group (Figure 53).

Figure 53: Notification rate for mumps, Australia, 2012, by age group and sex

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Cases of mumps were notified in most age groups, the median age at diagnosis being 30 years (range 1–84 years). The most notable increase in age group specific rates occurred among adults in the 20–39 years age group, although their overall rates in 2012 remained low compared with the peak experienced in this age group in 2007 to 2008 (Figure 54).

Figure 54: Notification rate for mumps, Australia, 2007 to 2012, by age group

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Indigenous status

Indigenous status was reported for 60% (n=120) of mumps cases in 2012, which was relatively consistent with the level of completeness over the previous 5-year period (mean 65%, range 51%–77%). Of these, 1 case was reported as being Indigenous.

Vaccination status

Of the 200 notified cases in 2012, 45% (n=89) were born after 1980 and were more than 12 months of age. This cohort was eligible for at least 1 dose of a publicly funded mumps-containing vaccine. In 2012, 64% (n=57) of cases were of unknown vaccination status and a further 20% (n=18) were unvaccinated. Of the remaining 16% (n= 14), 6 cases were fully vaccinated having received 2 doses of a mumps vaccine and 4 cases were partially vaccinated with 1 dose of a mumps vaccine. Four cases were reported as having been vaccinated with no information on the number of doses provided.

Discussion

The mumps component of the MMR vaccine is considered to be the least effective of the 3 components. This is based on outbreak investigations and post marketing studies that report that 1 dose of vaccine provides 60%–90% protection, which varies depending on the virus strain used in the vaccine.^75–77 Outbreaks have been reported among 2 dose recipients, particularly young adults who received their vaccines more than 10 years previously, suggesting that 2 doses may not be sufficient to prevent outbreaks in this cohort.^78,79 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.⁸⁰

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Pertussis

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 previous infection.⁸¹ 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.¹⁹

The NIP schedule in 2012 included a primary course of 3 doses of vaccine at 2, 4, and 6 months of age, with additional booster doses at 4 years and between 10 and 15 years of age, the latter being delivered through school based programs.²⁰

Epidemiological situation in 2012

In 2012, there were 24,069 notifications of pertussis including 2 deaths in infants aged less than 8 weeks who were too young to be vaccinated. Although declining, there continued to be large numbers of cases associated with the Australia-wide epidemic that began in mid-2008 and peaked in early 2011 (Figure 55). While pertussis remains endemic in Australia with a cyclical pattern of epidemic activity occurring approximately every 3–4 years, this most recent epidemic has been much larger and more prolonged than previous outbreaks (Figure 56).

Figure 55: Notifications and notification rates for pertussis, Australia, 1993 to 2012

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Figure 56: Notifications of pertussis, Australia, 2007 to 2012, by month and year of diagnosis and and state or territory

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In 2012, jurisdiction specific rates varied considerably with the Australian Capital Territory (225 per 100,000), Queensland (201 per 100,000) and New South Wales (181 per 100,000), all having notification rates higher than the national notification rate (173 per 100,000) (Figure 57). Since 2008, the timing of epidemic activity has varied across all jurisdictions. In all states and territories, except Tasmania, notification rates decreased in 2012 compared with 2011. In Tasmania, the notification rate increased more than 3-fold, from 69 per 100,000 in 2011 to 249 per 100,000 in 2012 (Figure 57). Between 2008 and 2012, multiple outbreaks, varying by geographical location, size and timing across jurisdictions, were the main cause of the varying rates for this period.

Figure 57: Notification rates for pertussis, 2007 to 2012, by state or territory

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Age and sex distribution

Following the peak in pertussis notifications in 2011, notifications decreased across all age groups in 2012. The highest notification rates were in children less than 15 years of age (236 per 100,000), accounting for 42% of all notifications. The highest age specific notification rate occurred in the 5–9 years age group (Figure 58). This was consistent with the overall trend of higher notification rates among children during the recent epidemic period, but differs from the trends observed prior to the epidemic in which children had much lower rates relative to adolescents and adults.

Figure 58: Notification rate for pertussis, Australia, 2007 to 2012, by age group and sex

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In 2012, females accounted for 56% (n=13,497) of cases, resulting in a male to female ratio of 1.2:1. Females had higher rates across all age groups, except adults aged 80 years or over (Figure 59). The highest notification rate for both males and females occurred in the 5–9 years age group (255 and 300 per 100,000 respectively) (Figure 59). In the 25–44 years age groups notification rates in females were more than 2 times that of males, which was likely due to the generally higher health seeking behaviour among adult females compared with males.⁸²

Figure 59: Notification rate for pertussis, Australia, 2012, by year age group

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Vaccination status

In order to determine the vaccination status of cases, public health follow up is required. States and territories prioritise case follow up to those less than 5 years of age.⁸³

In response to the ongoing epidemic in 2012, some infants were provided their first vaccination at 6 weeks of age and young children their fourth from 3.5 years. During 2012, those aged less than 5 years and eligible for a pertussis-containing vaccine, accounted for 13% of all notified cases and information about vaccination status was available for 91% of these cases.

Of the children eligible to have received their full primary course, 52% (n=1,172) had received their scheduled 3 vaccinations and 37% (n=164) had received their full scheduled course of 4 doses (Table 19).

Table 19: Notifications of pertussis in persons aged 0–5 years, Australia, 2012, by age group and number of doses of vaccine*

Age group	Number of vaccine doses					Unknown	Total
	0	1	2	3	4
* Excludes 6 notifications for whom age in months could not be determined.
Less than 6 weeks of age (not eligible for vaccination)	47					42	89
6 weeks to <4 months (eligible for 1 dose of vaccine)	51	141	4			35	234
4 to < 6 months (eligible for 2 doses of vaccine)	21	66	41			8	136
6 months to < 4 years (eligible for 3 doses of vaccine)	205	468	259	1,150	22	154	2,255
4 to 5 years (eligible for 4 doses of vaccine)	51	75	44	74	164	38	446
Total	375	750	348	1,224	186	277	3,160

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During the recent epidemic period between 2008 and 2012, there were 10 pertussis associated deaths reported to the NNDSS all of whom were 8 weeks of age or less. Two of these cases had received 1 dose of a pertussis containing vaccine.

Discussion

In Australia, epidemics of pertussis have historically occurred at regular intervals of approximately 4 years on a background of endemic circulation.⁸⁴ The timing of the recent multi-year epidemic was not uniform across the country with the Australian Capital Territory, Queensland, New South Wales, Victoria and Western Australia all experiencing their highest notification rates in 2011 while the Northern Territory, South Australia and Tasmania experienced peak levels of pertussis in 2008, 2010 and 2012 respectively.

The most important factors that have likely contributed to the baseline increase include more sensitive diagnostic techniques,^85,86 increased awareness and testing for pertussis in adolescents and adults, reduced effectiveness of the newer acellular vaccines,^87–89 and the removal of the 18-month booster dose from the routine schedule in 2003.⁹⁰

Strategies to reduce pertussis infection in young children, particularly among those less than 6 months of age continued in 2012. States and territories continued to provide ongoing public awareness campaigns including extended funding during 2012 for a ‘cocooning’ program giving booster vaccinations to pregnant women, parents and carers of infants. The Australian Technical Advisory Group on Immunisation also recommend bringing forward the 1st dose of the pertussis containing vaccine from 8 weeks to 6 weeks and scheduling the 5th (adolescent booster) dose at 11–13 years of age to better protect siblings, especially newborns, in response to outbreak settings.⁹¹

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Poliomyelitis

Poliomyelitis is a highly infectious disease caused by gastrointestinal infection with poliovirus. Transmission occurs primarily from 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).¹⁹

Vaccines formulated with inactivated poliovirus, are available in combination with diphtheria toxin, tetanus and other antigens. The NIP schedule in 2012 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.²⁰

In 2012, there were no notifications of poliomyelitis. The last case of poliomyelitis was an imported case in 2007. There has not been a case caused by a locally acquired wild poliovirus in Australia since 1972.

Australia, along with the WHOs Western Pacific Region, remains poliomyelitis free. Clinical and laboratory investigation is conducted for all cases in patients 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 Australia has achieved in all years since 2008. More details can be found in the annual reports of the Australian National Enterovirus Reference Laboratory published in CDI.⁹²

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Rubella

Rubella is generally a mild self-limiting viral 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 cause a fever and 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 manifest as foetal malformation or result in the death of the foetus.¹⁹

The main aim of immunisation for rubella is to prevent cases of CRS.⁹³ Rubella vaccine is included in the combined MMR vaccine. In 2012, it was provided under the NIP schedule at 12 months and 4 years of age.²⁰

Epidemiological situation in 2012

In 2012, 36 notifications of rubella were reported, representing a notification rate of 0.16 per 100,000 and a decrease compared with 2011 (n=58) and the 5-year mean. Cases were reported from all jurisdictions except the Northern Territory in 2012 (Table 4) (Figure 60). There was 1 case of CRS reported in 2012. Indigenous status was recorded for all cases; and none were reported as being Indigenous.

Figure 60: Notifications of rubella, Australia, 2007 to 2012, by month of diagnosis

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Age and sex distribution

The male to female ratio in 2012 was 1.1:1 comprising 19 males and 17 females. The highest rates for females occurred in the 25–29 years age group (0.96 per 100,000) and for males in the 30–34 years age group (0.88 per 100,000) (Figure 61).

Figure 61: Notification rate for rubella, Australia, 2012, by age group and sex

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The majority of cases (69%) continued to occur among adults aged 20–39 years, with a median age of 31 years (Figure 62).

Figure 62: Notification rate for rubella, Australia, 2007 to 2012, by age group

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Vaccination status

Of the 36 cases notified in 2012, 64% (n=23) were of unknown vaccination status and 19% (n=7) were reported as being unvaccinated. The remaining 6 cases were reported as having been vaccinated. Of these five were partially vaccinated having received 1 dose of a rubella-containing vaccine and 1 case had no vaccine dose information provided.

The vaccination status of those cases in women of child-bearing age and in adult men was unknown in most cases. Of the 11 female cases 15–44 years of age and the 16 adult males, four were reported as having been vaccinated, two were partially vaccinated and for two the number of vaccine doses was not reported.

Source of infections

In 2012, almost a quarter of rubella virus infections (n=8) were imported from overseas. There were three each from India and Indonesia, and one each from Germany and South East Asia. A 3rd of cases were reported as having been acquired in Australia. The place of acquisition was not reported for the remaining 44% of cases.

Discussion

Goals for the elimination of rubella and CRS have been set by a number of World Health Organization regions. Elimination has been declared by the Pan American Health Organization. The WHO Western Pacific Region, of which Australia is a member, has set goals for increased rubella and CRS elimination efforts, including the strengthening of immunisation and surveillance activities to confirm the absence of endemic strains.

Evidence suggests that rubella is well controlled in Australia. Measures implemented in the late 1990s under the Measles Control Campaign, which included lowering the age for the 2nd dose of the combined MMR vaccine to 4 years and a catch-up program, resulted in high levels of vaccine coverage and sustained low incidence of rubella disease since that time. Now almost a quarter of infections are imported from overseas. Young men, historically a more susceptible cohort due to the delayed introduction of universal vaccination, no longer appear to be at greater risk of infection compared with females. However, the majority of cases, although small, continue to occur among adults of child-bearing age.

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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 manured soil.¹⁹ 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.

Tetanus vaccination stimulates the production of antitoxin, which protects against the toxin produced by the organism. Tetanus toxoid is available in combination with diphtheria and other antigens. The NIP schedule in 2012 recommends 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. Booster doses are recommended for all adults at the age of 50 years who have not received a booster dose in the previous 10 years.

Epidemiological situation in 2012

In 2012, there were 7 notifications of tetanus, which was consistent with the low numbers seen in recent years. As laboratory confirmation of tetanus is usually not possible, notification of cases relies on reports from clinicians, resulting in the potential for under-reporting.⁴⁵ Indigenous status was complete for 6 of the 7 cases. None of these cases were reported as being Aboriginal or Torres Strait Islander (Figure 63).

Figure 63: Notifications of tetanus, Australia, 2002 to 2012, by year of diagnosis

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Age and sex distribution and vaccination status

There were 2 male and 5 female cases reported in 2012. Two cases were in the 20–29 years age group and the remaining 5 cases were over 75 years of age. One case had received 1 dose of a tetanus containing vaccine, the remaining 6 cases were not vaccinated or were of unknown vaccination status. Two deaths occurred in unvaccinated adults over 75 years of age.

Discussion

Tetanus in Australia 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 is important in the elderly, as most deaths occur in those over 70 years of age, especially women, particularly given that the infection may be associated with a minor injury.²⁰

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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 (herpes zoster), which has a 20%–30% risk of occurring following reactivation of the latent virus. Shingles occurs more frequently among older adults (most commonly after 50 years of age) and in immunocompromised people.¹⁹

In 2006, CDNA agreed to the 3 categories of VZV infection being nationally notifiable: chickenpox, shingles and varicella infection unspecified. By 2009, all jurisdictions were notifying VZV 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 notifications nationally are reported as being unspecified.

An analysis of South Australian VZV infections, where the majority of cases are followed up to establish the clinical presentation, highlights that since 2006 notifications of clinically confirmed chickenpox have remained relatively stable overall with declining trends among those births cohorts targeted by vaccination. Over this period notifications of shingles have increased.

Epidemiological situation in 2012

In 2012, there were 14,898 VZV notifications from the 7 reporting jurisdictions. This was 7% higher than the number notified in 2011 (n=13,808). This upward trend in the total number of notifications has been observed since 2009 and is most likely due to increased awareness of the requirement to notify and diagnostic laboratory testing by health care practitioners. Of the total VZV notifications in 2012, 57% (n=8,453) of cases were reported as unspecified varicella infection, 30% (n=4,481) as shingles and 13% (n=1,964) as chickenpox (Figure 64).

Figure 64: Proportion of notified cases of varicella zoster virus unspecified, chickenpox and shingles, 2012, by state or territory*

* Excluding New South Wales.

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Chickenpox

Chickenpox is an illness due to a highly contagious virus, varicella zoster, which is spread by respiratory secretions, including aerosol transmission, or from the vesicle fluid of skin lesions from a patient with chickenpox or shingles. Chickenpox is usually a mild disease of childhood, but 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.²⁰

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.

Epidemiological situation in 2012

In 2012, there were 1,964 cases of chickenpox reported; a notification rate of 13 per 100,000 and a 6% decrease in the number of notifications compared with 2011 (n=2,099). The highest notification rate, 63 per 100,000, was reported from the Northern Territory (n=149), followed by South Australia, 29 per 100,000 (n=476), reflecting the higher case ascertainment in these jurisdictions.

Age and sex distribution

The male to female ratio in 2012 was 1:1.1, with a slight variation particularly in the older age groups where reported case numbers were small. Sixty-one per cent of notified chickenpox cases (n=1,185) occurred in children aged less than 10 years. The 5–9 years age group had the highest notification rate for both sexes (71 per 100,000 for males and 67 per 100,000 for females) (Figure 65). 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 of laboratory notified cases of younger children.

Figure 65: Notification rate for chickenpox, Australia,* 2012, by age group and sex

* Excluding New South Wales.

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Vaccination status

In 2012, the oldest cohort of children eligible for varicella vaccination at 18 months of age under the NIP would now be 8 years of age. The analysis of vaccination status is therefore restricted to this cohort. Vaccination status information was available for 54% (n=387) of cases in this cohort with 87% having been vaccinated (n=337) and 13% not vaccinated (n=50).

Shingles

Shingles occurs most commonly with increasing age, impaired immunity, and a history of chickenpox in the first year of life.²⁰ Reactivation of VZV resulting in 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.¹⁹

Zostavax is a live attenuated viral vaccine formulated from the same VZV vaccine strain as currently licensed varicella vaccines. However, it is of a higher potency that is designed to elicit a boost in the immune response for the prevention of VZV reactivation to cause shingles. 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.²⁰

Epidemiological situation in 2012

In 2012, there were 4,481 cases of shingles notified; a notification rate of 29 per 100,000 and similar to 2011. The highest rates of shingles occurred in South Australia, (106 per 100,000, n=1,761) followed by the Northern Territory, (78 per 100,000, n=183). The high rates in these jurisdictions likely reflect their higher levels of case ascertainment compared with other jurisdictions.

Age and sex distribution

The notification rate was lower in males at 26 per 100,000 compared with females at 33 per 100,000, representing a male to female ratio of 0.8:1.

As expected, rates increased with age with the highest rates in the 85 years or over age group for both males and females, at 67 per 100,000 and 82 per 100,000 respectively (Figure 66).

Figure 66: Notification rate for shingles, Australia,* 2012, by age group and sex

* Excluding New South Wales.

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Discussion

It is estimated that 150,000 new cases of shingles occur each year in Australia with the majority of cases in adults over 50 years of age.^{94– 96} Analysis of the South Australian data, where the majority of cases have been followed up to establish clinical diagnosis, shows an increase in shingles notifications since 2006. As noted for chickenpox, the increasing trend in shingles incidence, also observed in several other settings, is likely 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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Varicella zoster virus (unspecified)

Notifications of unspecified VZV are laboratory specimens that are positive for VZV but do not have the clinical diagnosis available to distinguish between chickenpox and shingles.

Epidemiological situation in 2012

In 2012, there were 8,453 cases of unspecified VZV infections reported, representing a notification rate of 55 per 100,000 and a 10% increase in notifications compared with 2011 (n= 7,691).

Geographical distribution

The highest notification rate for unspecified VZV was from Queensland at 97 per 100,000 (n=4,414) due to the mainly laboratory based notification of VZV in that state (Table 5). 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.

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 (59 cases per 100,000) compared with males (50 per 100,000), which is consistent across most age groups. The highest age group specific notification rates occurred in the 75–79 years age group for females (114 per 100,000) and in the 85 years or over age group for males (112 per 100,000). The lowest age group specific notification rates were in the 0–4 years age group for both males and females. This was likely reflecting increased jurisdictional follow up to determine clinical presentation in children of this age (Figure 67).

Figure 67: Notification rate for varicella zoster virus (unspecified), Australia,* 2012, by age group and sex

* Excluding New South Wales.

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