This article was published in Communicable Diseases Intelligence Vol 35 Number 2, June 2011 and may be downloaded as a full version PDF file (1854 KB).
Vaccine preventable diseases
This section summarises the national notification surveillance data for notifiable diseases targeted by the National Immunisation Program (NIP) in 2009. These include diphtheria, invasive Haemophilus influenzae type b infection, laboratory-confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease, poliomyelitis, rubella, tetanus and varicella zoster infections (chickenpox, shingles and unspecified). Data on hepatitis B and invasive meningococcal disease, which are also targeted by the NIP, can be found in this report under ‘Bloodborne diseases’ and ‘Other bacterial infections’ respectively. Other vaccine preventable diseases (VPDs) presented in this report include hepatitis A and Q fever under the ‘Gastrointestinal’ and ‘Zoonoses’ sections respectively. Rotavirus is not included as it is not a nationally notifiable condition. For more comprehensive reports on historical data, including notifications, hospitalisations and deaths, readers are referred to the regular CDI supplements Vaccine Preventable Diseases in Australia, the latest of which has recently been published.53
In 2009, there were 101,627 notifications of VPDs (43% of total) reported to the NNDSS. This was 2.9 times more notifications than in 2008 (33,983). Influenza was the most commonly notified VPD (58,778, 58% of total) followed by pertussis (29,736, 29% of total) reflecting the epidemics occurring as a result of these 2 diseases in 2009. The number of notifications and notification rates for VPDs in Australia are shown in Table 3 and Table 4, respectively.
There were no new vaccines added to the NIP in 2009. However, in response to the influenza pandemic experienced during 2009, a monovalent vaccine was developed and distributed through the national Pandemic (H1N1) 2009 Vaccination Program from the end of September 2009 to reduce transmission of the pandemic (H1N1) 2009 influenza virus and protect vulnerable individuals. Whilst the Program initially focused on particular priority groups, including health care workers and those vulnerable to severe health outcomes associated with influenza infection, the vaccine was also made available for free to everyone in Australia who wished to be vaccinated.
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 areas of lower coverage remain, in which there is a potential for VPDs to occur and circulate. These mainly coincide with high levels of conscientious objectors to immunisation including coastal areas of South East Queensland, northern New South Wales, Adelaide and south-western Western Australia. On average, just 3% of children in Australia are not fully vaccinated for age, but in the above areas this proportion is much higher.54
Information on receipt of vaccines has historically been recorded on NNDSS using the ‘vaccination status’ field (full, partial or unvaccinated), plus a field capturing the number of doses. In January 2008 new, more detailed fields were added to record ‘vaccine type’ and ‘vaccination date’ for each dose. The new fields were intended to replace the old fields, with a transition period allowing either form of vaccination details. In 2009, four jurisdictions were using the new fields (Northern Territory, Queensland, Tasmania and New South Wales for selected diseases), while the remaining jurisdictions continued to use the old fields. In this report data on receipt of vaccines is presented for each disease combining data from the two different formats. No vaccine is 100% effective, and therefore infections sometimes do occur in fully vaccinated people, and some are reported later in this section. However, effective vaccines do provide a substantially lower chance of becoming infected, and/or reduced severity of disease. Monitoring vaccine failure rates is an important part of evaluating the NIP.
Diphtheria is an acute illness caused by toxin-producing strains of the bacterium Corynebacterium diphtheriae. It normally involves the mucous membranes of the upper respiratory tract producing a membrane that can obstruct the airway. On rare occasions other mucous membranes or the skin can be affected. Diphtheria is spread by respiratory droplets or by direct contact with skin lesions or articles soiled by infected individuals.21
There were no notifications of diphtheria reported to NNDSS in 2009. The last notification of diphtheria reported in Australia was a case of cutaneous diphtheria (which affects the skin) in 2001, the only notification reported since 1992.
In April 2009, the WHO announced the emergence of a novel influenza A virus, prompting the declaration of the first public health emergency of international concern since the International Health Regulations (2005) came into effect in 2007. The WHO subsequently raised the pandemic influenza alert in June 2009 to phase 6, the pandemic phase. The first notification of the pandemic (H1N1) 2009 influenza virus in Australia occurred in May 2009.
During the pandemic response, influenza notifications were reported by each jurisdiction using NetEpi, a web-based outbreak case reporting system, in addition to NNDSS. A more detailed analysis of enhanced data collected through NetEpi and additional sentinel surveillance systems will be reported in the 2010 National Influenza Surveillance Scheme annual report. The number of notifications in the Australian 2009 influenza season was the highest since national reporting to the NNDSS began in 2001, and substantially higher than in recent years (Figure 39). In 2009, there were 58,562 notifications of laboratory-confirmed influenza, a rate of 268 cases per 100,000 population. The number of notifications was 8.6 times greater than the 5-year mean and peaked in July with 29,770 notifications, but this over-representation is likely, at least in part, to reflect testing and laboratory practices in addition to real differences in the incidence of infection.55 Notifications in the non-seasonal period were also higher than in previous years. Although Queensland continued to account for the highest proportion of all confirmed influenza cases notified (31%) (Figure 40), this figure was lower than previous years (the average for 2005–2008 was 44%, range 38%–54%). Throughout 2009, national testing protocols for each phase of the pandemic response were informed by the influenza SoNG. For example during the ‘Protect’ phase the influenza SoNG focused on the testing of persons most at risk for severe disease outcomes, including people belonging to identified vulnerable groups and those presenting with severe disease presentation. However, due to local influenza activity and resource availability, testing rates in jurisdictions were variable.
Figure 39: Notifications of laboratory-confirmed influenza, Australia, 2009, by month and year of diagnosis
Figure 40: Notifications of laboratory-confirmed influenza, Australia, 2009, by state or territory and week of diagnosis
In 2009, the highest notification rates occurred in the Northern Territory (875 per 100,000 population), followed by South Australia (663 per 100,000 population), Queensland (417 per 100,000 population) and the Australian Capital Territory (359 cases per 100,000 population) (Table 3).
In 2009, distribution of influenza notifications tended to occur in persons aged less than 55 years, with substantially higher rates observed in persons aged less than 30 years, compared with older age groups. In previous years, notifications of laboratory-confirmed influenza were highest in children aged 0–4 years (Figure 41), which represented, on average, 18% of notifications, whereas in 2009 they represented only 12% of notifications. In contrast, notification rates in 2009 were highest in the 5–9, 10–14 and 15–19 years age groups (Figure 42).
Figure 41: Notification rate for laboratory-confirmed influenza, Australia, 2006 to 2009, by age group
Figure 42: Notification rate for laboratory-confirmed influenza, Australia, 2009, by age group and sex*
* Excludes 128 notifications for whom age or sex were not reported.
In 2009, 58,411 (99.8%) influenza notifications in the NNDSS and NetEpi had typing data. Of the typed notifications, 64.6% (37,750) were pandemic (H1N1) 2009, 31.4% (18,345) were notified as influenza A not subtyped, 2.8% (1,612) were influenza A/H3N2, 0.7% (410) were influenza B and 0.5% (294) were influenza A/H1N1 (seasonal) (Figure 43).
Figure 43: Notifications of laboratory-confirmed influenza, Australia, 2009, by type and week of diagnosis*
* Notifications of influenza ‘untyped’ (n = 150) excluded from analysis.
In 2009, 1,586 influenza virus isolates were subtyped by the WHO Collaborating Centre for Reference and Research on Influenza (WHOCC), representing almost 3% of laboratory-confirmed cases reported to the NNDSS. Pandemic (H1N1) 2009 represented the majority (74%) of isolates subtyped, followed by influenza A(H3N2) (18%), seasonal A(H1N1) (7%) and influenza B (1%).
The WHOCC also conducted antigenic characterisation on 884 of the influenza virus isolates, in similar proportions to those subtyped. The majority of pandemic (H1N1) 2009 isolates were characterised as A/California/7/2009-like. Seasonal influenza A(H1N1) viruses of the 2009 vaccine, A/Brisbane/59/2007, circulated sporadically throughout the year in very low numbers, being displaced by the pandemic (H1N1) 2009 strain.56 Of the circulating influenza A(H3N2) viruses, most were antigenically similar to the 2009 A/Brisbane/10/2007 vaccine component, however the majority of these were low reactor versions indicating some drift in the strain. Although there were only a small number of influenza B viruses detected, antigenic characterisation showed a drift throughout the season in the 2009 vaccine strain, B/Florida/4/2006 (B/Yamagata lineage), to the B/Brisbane/60/2008 (B/Victoria lineage) strain.
All 3 strains in the 2010 Southern Hemisphere influenza vaccine were different to those previously recommended in the 2009 Southern Hemisphere vaccine. The 2010 vaccine contained A/California/7/2009 (H1N1)-like, A/Perth/16/2009 (H3N2)-like and B/Brisbane/60/2008-like viruses.
Antiviral susceptibility testing for resistance to oseltamivir or zanamivir by enzyme inhibition assay (EIA) was conducted on 587 isolates of the pandemic (H1N1) 2009 strain by the WHOCC during 2009. Of these isolates, four showed resistance to oseltamivir. Molecular analysis of 276 isolates found 9 isolates (including the 4 oseltamivir resistant isolates identified through EIA) with the H275Y mutation, which is known to confer resistance to oseltamivir. Oseltamivir resistance was also found in the majority (36 of 37) seasonal A/H1N1 isolates tested, which is consistent with historical trends. In 2009 there were no reports of antiviral resistance in any of the A(H3N2) or influenza B isolates tested.
Invasive Haemophilus influenzae type b disease
Invasive Haemophilus influenzae type b bacteria 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 in 1993, there has been a marked reduction in total Hib notifications in Australia (Figure 44), which now has one of the lowest rates of Hib notifications in the world.57
Figure 44: Notifications and rates for invasive Haemophilus influenzae type b infection, Australia, 1991 to 2009, by year of diagnosis
There were 19 notifications of Hib disease in 2009, a rate of 0.1 per 100,000 population, and six fewer than reported in 2008. Thirty-seven per cent (7) of notifications were amongst children less than 5 years of age with the majority of these (6/7) infants aged less than 1 year. The remaining 12 notifications ranged between 13 and 74 years. Fifty-eight per cent (11) were males resulting in a male to female ratio of 1.4:1. (Figure 45).
Figure 45: Notifications of invasive Haemophilus influenzae type b infection, Australia, 2009, by age group and sex
Indigenous status was 100% complete for notifications in 2009. Thirty-seven per cent (7/19) were reported as Indigenous and 63% (12/19) were non-Indigenous. The Hib notification rate in 2009 was 1.3 per 100,000 in Indigenous people and 0.1 per 100,000 in non-Indigenous people, a ratio of 13:1. Between 2004 and 2009, Hib rates for Indigenous people ranged between 5.5 and 30.3 times higher than for non-Indigenous people (Figure 46). However, these figures vary widely because of the low number of notifications. This analysis excludes those notifications with an unreported or unknown Indigenous status between 2004 and 2009 (4 for 2006 and 1 for each remaining year).
Figure 46: Notifications and rates for invasive Haemophilus influenzae type b infection, Australia, 2004 to 2009, by Indigenous status
All children under the age of 17 years in 2009 were eligible for Hib vaccination in infancy, as Hib vaccines were introduced to the NIP in April 1993 for all children born after February 1993. There were 9 notifications for children less than 17 years of age in 2009. The majority (7/9) of these were one year of age or less of which five were vaccinated and two were not vaccinated. Of the five who were vaccinated four had received 1 dose of a Hib containing vaccine and one had received 2 doses. Although four of these 5 vaccinated cases had received their age appropriate dose of vaccine none of the five had received the full course of recommended vaccine, which includes 3 or 4 doses depending on Indigenous status. The remaining two were a 13-year-old who had received 3 doses and a 14-year-old with unknown vaccination status.
Invasive pneumococcal disease
There were 1,559 notifications of invasive pneumococcal disease (IPD) in Australia in 2009, a rate of 7.1 notifications per 100,000 population. This was a small decrease of 4% from the 1,634 reported in 2008 (7.6 per 100,000). An increase in rates in 2009, compared with 2008, was seen in the Australian Capital Territory (29, 8.3 per 100,000), the Northern Territory (86, 38.2 per 100,000), South Australia (145, 8.9 per 100,000) and Victoria (368, 6.8 per 100,000). A decrease in notifications was noted in Queensland (270, 6.1 per 100,000), New South Wales (477, 6.7 per 100,000), Tasmania (35, 7.0 per 100,000), and Western Australia (149, 6.7 per 100,000).
In 2009, males accounted for 54% (843) of the 1,559 notifications of IPD. In most age groups there were more male than female notifications, resulting in a male to female ratio of 1.2:1. Figure 47 shows that the highest rates of IPD in 2009 were notified in persons aged 85 years or over (32.3 per 100,000) and in children aged 1 year (26.2 per 100,000).
Figure 47: Notification rate for invasive pneumococcal disease, Australia, 2009, by age group and sex
In 2001, the 7vPCV became available for infants and children at high risk of IPD, including Indigenous infants. In 2005 it was added to the NIP for all children up to 2 years of age.12 Rates of IPD disease caused by 7vPCV serotypes have declined between 2004 and 2009 from 7.7 to 1.0 per 100,000 (1,548 to 216 notifications). The decline was seen across all age groups (Figure 48). Those aged 65 years or more had the greatest rate of IPDs caused by 7vPCV serotypes in 2009 (72, 2.5 per 100,000) with those aged less than 2 years having a rate of 1.9 per 100,000 (11 notifications).
Figure 48: Notification rate for invasive pneumococcal disease caused by 7vPCV serotypes, Australia, 2002 to 2009, by age group
Additional data were collected on notifications of IPD in all Australian jurisdictions during 2009. More detailed analyses can be found in the IPD annual report series published in CDI.
Measles is a highly infectious, acute viral illness spread by respiratory secretions, including air-borne transmission via aerosolised droplets. The prodrome, lasting 2 to 4 days, is characterised by fever and malaise followed by a cough, coryza and conjunctivitis. It is usually followed by a maculopapular rash, which typically begins on the face, and then becomes generalised. Measles can be a severe disease, with complications such as otitis media, pneumonia, and acute encephalitis. Subacute sclerosing panencephalitis (SSPE) is a late, rare (approximately 1 in 100,000 cases) complication of measles,21 which is always fatal.12 Evidence suggests that endemic measles has been eliminated from Australia, since at least 2005.58
There were 104 notifications of measles reported to NNDSS in 2009, representing a rate of 0.5 notifications per 100,000 population. This represents an increase from the 65 notifications reported in 2008 (0.3 notifications per 100,000 population) and the 12 reported in 2007 (0.1 per 100,000) (Figure 49). In 2009, notifications were reported from all states and territories: Victoria (36), Queensland (32), New South Wales (19), Western Australia (10), South Australia (3), Tasmania (2), the Australian Capital Territory (1) and the Northern Territory (1).
Figure 49: Notifications of measles, Australia, 2004 to 2009, by month and year of diagnosis
In 2009, 63% (66/104) of measles notifications were male. The age at diagnosis ranged from 6 months to 56 years with the median age being 16 years. There was an increase in notifications in three age groups (5–14 years, 15–24 years and 25–34 years) compared with 2008, while the remaining three age groups (< 1 year, 1–4 years and 35+) remained relatively constant compared with 2008 (Figure 50). This increase was highest in the 5–14 years age group with 36 notifications in 2009 compared with 14 in 2008; in part influenced by an outbreak in a Sunshine Coast High School in Queensland, in which 18 cases were in this age group.
Figure 50: Notifications of measles, Australia, 2004 to 2009, by age group and year of diagnosis
In 2009, 34% (35/104) of notifications were reported as being acquired from overseas including: Vietnam (11), India (6), Thailand (4), the Philippines (2), the United Kingdom (2), the United States of America (2), New Zealand (2) and 1 importation each from Iran, France, South Africa, China, Indonesia and Korea. Of the remaining 69 locally-acquired cases, 62 were epidemiologically linked to the imported cases. There were 3 outbreaks with more than 5 cases during 2009: one with 25 cases in a Sunshine Coast high school in Queensland that was linked to an imported case from India, one with 20 cases in Victoria that was also linked to an imported case from India, and one with 11 cases in Victoria that was linked to an imported case from Iran. Seventy-six of the 104 cases were linked to specific genotypes of which 29 were identified as D4, 26 as D8, 19 as H1 and 2 as D9.
Two doses of the MMR vaccine are funded under the NIP for children and provided at 12 months and 4 years of age. The MMR induces long-term measles immunity in 95% of recipients after a single dose and 99% of recipients after the 2nd dose.12
Nationally, there was information on vaccination for 70% (73/104) of notifications in 2009 of which 85% (62/73) were not vaccinated and 15% (11/73) had been vaccinated (1 with 2 doses and 9 with 1 dose and the remaining 1 case with no dose number stated; Figure 51). There were 6 notifications in infants less than 1 year of age at diagnosis who were ineligible for routine vaccination. Only one of the 4 cases in children between one and 3 years of age, who were eligible for 1 dose of the MMR, were vaccinated. Fifty-four notifications with vaccine information available were between four and 26 years of age and eligible for 2 doses of MMR. Ninety-one per cent (49/54) of those were not vaccinated and 9% (5/54) had been vaccinated. Two of those vaccinated in this age group had 2 doses and 2 cases had 1 dose of a measles-containing vaccine and the remaining case had no dose number stated. There were 10 notifications with information on vaccination in the 27–41 years age group. This age group is considered to be a susceptible age cohort because many may have missed being vaccinated as infants when coverage was still low and the risk of natural immunity through exposure was declining. Of these, 50% were not vaccinated. Of the 5 vaccinated cases in this age group, four had 1 dose and the additional case had no dose number stated. The remaining 1 notification was in the 42 years or over age group and not vaccinated.
Figure 51: Notifications of measles, Australia, 2009, by age group and vaccination status
Mumps is an acute viral illness transmitted by the respiratory route in the form of air-borne droplets or by direct contact with saliva of an infected person. A high proportion of mumps infections involve non-specific symptoms including fever, headache, malaise, myalgia and anorexia with approximately one-third of infections being asymptomatic. The characteristic bilateral, or occasionally unilateral, parotid swelling occurs in 60% to 70% of clinical cases.21
In 2009, there were 165 notifications of mumps (0.8 notifications per 100,000 population), compared with the 285 notifications (1.3 per 100,000) reported in 2008 (Figure 52) and a ratio of 0.6 compared with the 5-year mean. The crude national rate has continued to decrease in 2009 after increasing from 2004 and peaking in 2007 at 2.8 per 100,000 (Figure 53).
Figure 52: Notifications of mumps, Australia, 2004 to 2009, by state or territory and month of diagnosis
Figure 53: Notification rate for mumps, Australia, 2004 to 2009, by age group
Notifications in 2009 were reported from all jurisdictions except the Australian Capital Territory, with 27% (45/165) from Victoria, 24% (40/165) from New South Wales and 21% (34/165) from Queensland. The highest rate was in the Northern Territory with 5.8 notifications per 100,000 population (13 notifications) followed by Western Australia with 0.9 per 100,000 (20 notifications).
There were no large mumps outbreaks in 2009. There were 2 small clusters notified to the NNDSS, the 1st involving 6 locally-acquired cases in Victoria and the 2nd was a localised cluster of 8 cases in a small country town in the Northern Territory.
In 2009, there were notifications of mumps in all age groups with the highest rates amongst adolescents (15–24 years) and young adults (25–34 years; Figure 53) reflecting historical vaccination schedules. Adolescents aged 15–24 years were eligible for 2 doses of a mumps-containing vaccine; however, coverage with the 2nd dose may have been suboptimal for some members of this cohort as they would have no longer been in primary school during the 1998 Measles Control Campaign (MCC). Only a small proportion of the young adults aged 25–34 years would have been eligible for 2 doses of a mumps-containing vaccine, and many would not have been eligible for 1 dose. However, some of this cohort would have developed natural immunity as exposure to wild virus was still likely when they were young children.59
In 2009, the highest rates were for males in the 20–24 and 25–29 years age groups (Figure 54), which is similar to 2008. Sixty per cent of notifications (99/165) were male, which is a similar proportion to the 5-year mean.
Figure 54: Notification rate for mumps, Australia, 2009, by age group
Indigenous status was reported for 65% (107/165) of mumps notifications, of which 90% (96/107) were reported as non-Indigenous and 10% (11/107) as Indigenous. This represents a 40% decrease in the proportion of Indigenous vs non-Indigenous notifications in 2009 compared with 2008 in which 50% were reported as Indigenous. The higher rate of Indigenous notifications in 2008 was influenced by an outbreak amongst Indigenous communities in the Kimberley region of Western Australia and the Northern Territory.60
The mumps component of the MMR vaccine has been estimated to be the least effective of the 3 components ranging from providing 62%–88% and 85%–95% protection for the 1st and 2nd dose respectively.61, 62 Reduced effectiveness of the mumps vaccine has been demonstrated over time such that waning immunity may at least partially account for the proportion of vaccinated mumps cases, and contribute to mumps outbreaks in older vaccinated populations.62
Nationally, information on vaccination was available for 34% (56/165) of the notifications, of which 59% (33/56) were not vaccinated and 41% (23/56) were vaccinated. The remaining 66% (109/165) were reported as not applicable or unknown. Of the vaccinated notifications 26% (6/23) had 2 doses and 43% (10/23) reported one dose of a mumps-containing vaccine, with the remaining seven having dosage information missing or unknown. Nine of the 11 Indigenous notifications had a reported vaccination status of which 89% (8/9) were vaccinated, one with 2 doses and seven with 1 dose of a mumps-containing vaccine, and one was not vaccinated.
Pertussis is the most common vaccine preventable illness in Australia after influenza. It is a highly infectious disease caused by Bordetella pertussis and spread by respiratory droplets. Epidemics occur at regular intervals of approximately 3 to 4 years, which can vary from region to region, on a background of endemic circulation. In vaccinated populations these outbreaks tend to be smaller with less mortality and morbidity than in unvaccinated populations.21 While pertussis can affect people of any age, infants are at highest risk of more severe disease as maternal antibody does not provide reliable protection and adequate immunity is not achieved through vaccination until receiving a 2nd dose at 4 months of age.63 The majority of notifications usually occur in the spring and summer months.
In 2009, 29,736 notifications of pertussis including 2 deaths were reported to NNDSS. This represents a notification rate of 135.9 notifications per 100,000 population, a 2-fold increase in notifications compared with 2008 (14,285; 66.7 per 100,000) and 3 times the 5-year mean (9,764). Both deaths were in infants less than 2 months of age and too young to be protected by vaccination. The increase in notifications reflects the Australia-wide epidemic that began in mid-2008. (Figure 55). The causes of this epidemic are unclear but contributing factors may include suboptimal vaccine coverage, improved testing methods and case finding, and waning immunity levels in the vaccinated population.
Figure 55: Notifications of pertussis, Australia, 2004 to 2009, by state or territory and month of diagnosis
In response to the nation-wide outbreak, many states and territories implemented public awareness campaigns and funded a booster vaccination program for parents of infants as part of a cocooning strategy to protect vulnerable infants from infection. These jurisdictions included Victoria and Queensland (for parents), the Northern Territory (for parents, carers and siblings of babies under 7 months of age), New South Wales (for parents, grandparents and other carers of infants) and the Australian Capital Territory (for parents and grandparents).
The government convened a Pertussis Working Party of the Australian Technical Advisory Group on Immunisation (ATAGI) in February 2009 to review the NIP schedule in light of the epidemic. ATAGI is continuing to consider all the available scientific evidence including options to optimise protection for babies in particular.
Notification rates in 2009 varied widely with age. Children aged less than 15 years had a higher rate of infection (271.8 notifications per 100,000 population) than those adolescents and adults 15 years of age or over (103.8 per 100,000) giving a rate ratio of 2.6. While this was similar to the 2008 rate ratio of 2.2, it contrasts markedly with the 2007, 2006, and 2005 rate ratios of 0.7, 0.3 and 0.5 respectively, reflecting the higher rate in adults relative to children during those years.
The highest rates amongst children were in infants less than 1 year of age (377.5 notifications per 100,000 population) followed by those aged 5–9 years (293.5 per 100,000) and those aged 1–4 years (277.5 per 100,000). This trend reflects that of 2008 but contrasts with 2007 when age group rates were more closely clustered.
Between 2004 and 2007, a period inclusive of the last national epidemic in 2005/2006, age group notification rates were either trending down or remaining relatively constant but since 2007 rates have been increasing. This increase is most marked amongst those less than 15 years of age (Figure 56).
Figure 56: Notification rate for pertussis, Australia, 2004 to 2009, by age group
Fifty-seven per cent (16,858/29,736) of notifications in 2009 were female and 43% (12,837/29,736) were male, 41 had no sex specified (Figure 57). The highest rate amongst females was in the 5–9 years age group (336.1 per 100,000 population) with the highest rate in males being in the 0–4 years age group (293.0 per 100,000). While rates for both sexes were highest in those aged less than 15 years, the pattern of predominance of female notification rates compared with males occurred in all age groups except for those aged 75 years or over.
Figure 57: Notification rate for pertussis, Australia, 2009, by age group and sex
Follow-up is required in order to determine the vaccination status of individual cases. In a large outbreak, follow-up of all cases is not possible and as per national guidelines, jurisdictions prioritised follow-up to those less than 5 years of age. This age group made up 14% (4,266/29,736) of all notifications in 2009.
While the pertussis vaccine is not 100% effective and does not confer life-long immunity, vaccine effectiveness is estimated to be 68% after receiving 1 dose of vaccine, increasing to 92% after the 2nd dose,64 and greater than 99% following subsequent doses.65 Immunity to disease decreases over time post vaccination with estimates of protection remaining for 4–12 years.64 The current vaccine schedule for pertussis under the NIP includes a dose provided at 2, 4 and 6 months of age followed by a booster at 4 years of age and again at 12–17 years of age (the timing of this last booster dose varies by jurisdiction).
Nationally, information on vaccination was available for 86% (3,676/4,266) of all notifications in children less than 5 years of age of which 80% (2,937/3,676) had received at least 1 pertussis containing vaccine and 18% (658/3,676) were not vaccinated. No data were entered or vaccination status was unknown for 14% (590/4,266) of the total notifications in this age group.
Of those 1,126 notifications less than one year of age, 54% (604/1,126) were vaccinated of which 41% (245/604) had received two or more doses of a pertussis vaccine. Twenty-one per cent (236/1,126) were less than 6 weeks of age and too young for their first scheduled dose of vaccine at 2 months.
Of 1,270 notifications for children aged between 3.5 and less than 5 years of age eligible for the first booster dose, only 15% (194/1,270) were reported as having had this 4th dose.
Pertussis notification rates varied considerably by state or territory and residential location. By jurisdiction, rates were highest in South Australia (5,346, 329.4 notifications per 100,000 population) followed by New South Wales (12,436, 175.2 per 100,000), Queensland (6,216, 141.1 per 100,000), Tasmania (616,122.6 per 100,000), the Australian Capital Territory (351, 99.9 per 100,000), the Northern Territory (215, 95.6 per 100,000), Victoria (3,778, 69.6 per 100,000) and Western Australia (778, 34.8 per 100,000).
Rates by SD also varied widely across most jurisdictions except for South Australia where they were uniformly high (Map 3). In New South Wales rates were highest in the Illawarra SD (1,505 notifications, 349.1 notifications per 100,000 population), with high rates also reported from coastal, north and central western areas. In Queensland rates were highest in the Northern SD (485, 213.3 per 100,000) followed by the Sunshine Coast (637, 197.0 per 100,000). The East Gippsland and Ovens-Murray SDs had the highest rates in Victoria (173 and 166 respectively, 199.3 and 166.2 per 100,000), while in Tasmania, the Southern and Greater Hobart SDs had the highest rates (87 and 363 respectively, 232.3 and 171.2 per 100,000). Western Australia’s rates remained low compared with the rest of Australia in 2009. Rates by SD should be interpreted with caution, as they can be high or low depending on the size of the population.
Map 3: Notification rates and counts* for pertussis, Australia, 2009, by Statistical Division of residence and Statistical Subdivision for the Northern Territory
* Numbers shown in the Statistical Divisions and Statistical Subdivisions represent the count of notifications.
Poliomyelitis is a highly infectious disease caused by gastrointestinal infection by a 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).21
In 2009, there were no notifications of poliomyelitis in Australia, which along with the Western Pacific Region remained poliomyelitis free. Poliomyelitis is a notifiable disease in Australia with clinical and laboratory investigation conducted for cases involving patients of any age with a clinical suspicion of poliomyelitis. Australia follows the WHO protocol for poliomyelitis surveillance and focuses on investigating cases of AFP in children under 15 years of age. The WHO target for AFP surveillance in a polio non-endemic country is 1 case of AFP per 100,000 children aged less than 15 years. Between 1 January and 31 December 2009 there were 54 eligible AFP cases notified to the National Polio Reference Laboratory (NPRL) of which all were classified as non-poliomyelitis. The 2009 non-poliomyelitis AFP rate was 1.17 hence meeting the WHO AFP surveillance indicator for the 6th time since 1995. Details of the 2009 notifications are provided in the 2009 annual report of the Australian NPRL.66
Rubella is generally a mild and self-limiting viral infectious disease. It is spread from person to person through direct contact with respiratory secretions or via air-borne droplets. Clinically, rubella can be difficult to distinguish from other diseases that cause a febrile rash, such as measles, and is asymptomatic in up to 50% of cases. Rubella infection in pregnancy can cause foetal infection resulting in congenital rubella syndrome (CRS). CRS occurs in up to 90% of infants born to women who are infected during the first 10 weeks of pregnancy and may result in foetal malformations and death.21
In 2009, there were 27 notifications of rubella (0.1 notifications per 100,000 population), a decrease compared with the 36 notifications in 2008. Notifications were reported from New South Wales (7), Victoria (6), Queensland (6), Western Australia (5) and South Australia (3). The age profile of rubella notifications in 2009 was similar to 2008. There were small numbers of notifications reported across the age groups with none in infants less than 1 year of age or for adults over 60 years of age (Figure 58). The median age was 29 years and 74% (20/27) of notifications were adults between 20 and 49 years of age. The overall male to female ratio of notified cases in 2009 was 1.7:1, (17 males and 10 females). Of the 10 females, 80% were notified in women of child-bearing age (17–47 years). There were no notifications of CRS reported in 2009.
Figure 58: Notifications of rubella, Australia, 2009, by age group and sex
Figure 59 shows that rubella notifications in different age groups have continued to trend at low levels since 2004, except for a spike amongst the 25–34 years age range in 2006. This spike was primarily due to an increase of notifications from the South Eastern and Central Sydney SDs in New South Wales. It was concentrated in those aged 15–44 years, however there was no single identifiable source for the increase in notifications.67
Figure 59: Notifications of rubella, Australia, 2004 to 2009, by age group
A single dose of rubella vaccine produces an antibody response in more than 95% of recipients and while antibody levels are lower than after natural infection, they are shown to persist for at least 16 years in the absence of endemic disease.12 Rubella vaccine is included in the combined MMR vaccine and provided under the NIP at 12 months and 4 years of age.
Nationally, information on vaccination was available for 48% (13/27) of rubella notifications of which the majority, 62% (8/13), was not vaccinated and 38% (5/13) were vaccinated. The remaining 52% (14/27) were stated as either unknown or blank. Of the 8 male notifications with information on vaccination reported, 71% (5/8) were not vaccinated, all of whom were adults in the 18–44 years age range, and three had received 1 dose of a rubella-containing vaccine. Of the 5 female notifications in 2009 with vaccination information reported, 60% (3/5) were not vaccinated (two were women of child-bearing age: 17-year-old and 24-year-old) and two had received at least 1 dose of a rubella-containing vaccine (4-year-old and 40-year-old).
None of the rubella notifications in 2009 was identified as Indigenous, although seven of the 27 were of unknown status.
Tetanus is an acute, often fatal, disease caused by the toxin produced by the bacterium Clostridium tetani. Tetanus spores usually enter the body through contamination of a wound with soil, street dust or animal or human faeces.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. Early symptoms and signs include increased tone in the jaw muscles, difficulty in swallowing, stiffness or pain in the neck, shoulder and back muscles. In Australia, tetanus is rare, occurring primarily in older adults who have never been vaccinated or were vaccinated in the remote past.12
Tetanus vaccination stimulates the production of antitoxin, which protects against the toxin produced by the organism. Complete immunisation (3 primary doses and 2 boosters included for children on the NIP) induces protective levels of antitoxin lasting throughout childhood, but by middle age about 50% of vaccines have low or undetectable levels. It is recommended, though not funded under the NIP, that all adults who reach the age of 50 years and have not received a booster of a tetanus-containing vaccine in the previous 10 years, should have one.12
In 2009, there were 3 notifications of tetanus, two from New South Wales and one from Victoria, all over 34 years of age. Of the 3 notifications, 2 male and 1 female, one had been partially vaccinated with 1 dose and the remaining two had no vaccination status recorded.
Varicella zoster virus infections
Chickenpox (also known as varicella) and shingles (also known as herpes zoster) are both caused by the varicella-zoster virus (VZV). VZV is a member of the herpesvirus family and is highly contagious. Chickenpox occurs on initial infection with the virus. The virus then stays dormant in the body’s nerve cells and has a 20%–30% chance of reactivating as shingles later in life.21
In November 2005, the varicella-zoster vaccine was added to the NIP schedule as a single dose due at 18 months (for children born on or after 1 May 2004), or as a catch-up dose at 10–13 years of age. In 2006, the Communicable Diseases Surveillance Network Australia (CDNA) agreed to make 3 categories of VZV infection notifiable: chickenpox, shingles and varicella infection (unspecified). The year 2009 was the first complete year in which all jurisdictions, except New South Wales, sent VZV data to NNDSS.
In 2009, there were 11,235 VZV notifications from the 7 reporting jurisdictions. This was 10% more than in 2008. Sixty-two per cent (6,977) were unspecified varicella infection, 14% (1,599) were chickenpox and 24% (2,659) were shingles.
Varicella-zoster virus infection (unspecified)
Notifications of unspecified VZV infections are laboratory specimens that are positive for VZV but have not been followed up by the local health authority and distinguished clinically as either chickenpox or shingles. Although varying by jurisdiction (Figure 60), VZV (unspecified) accounted for 62% of all VZV notifications in 2009, an increase compared with 52% of the total in 2008.
There were 6,977 notifications of VZV infections (unspecified) based on laboratory diagnoses compared with 4,415 in 2008, with a rate of 47.2 notifications per 100,000 population. The high proportion of unspecified VZV infection compared with chickenpox or shingles is attributable to the varying capacity of jurisdictions to follow-up on laboratory notifications to determine the clinical presentation of each case. The highest rates were reported from Queensland (3,835 notifications, 87.0 per 100,000 population), Western Australia (866, 38.7 per 100,000) and Victoria (1,847, 34.0 per 100,000).
Figure 60: Proportion of total notifications for varicella-zoster virus unspecified, chickenpox and shingles, 2009, by state or territory*
* Excluding New South Wales.
The age and sex distribution of unspecified VZV are shown in Figure 61.
Figure 61: Notification rate for varicella-zoster virus unspecified, Australia,* 2009, by age group and sex
* Excluding New South Wales.
Chickenpox is a highly contagious infection spread by air-borne transmission of droplets from the upper respiratory tract or from the vesicle fluid of the skin lesions of chickenpox or shingles infections. Chickenpox is usually a mild disease of childhood, however complications occur in approximately 1% of cases. It is more severe in adults and in individuals of any age with impaired immunity, in whom complications, disseminated disease, and fatal illness can occur.12
In 2009, there were a total of 1,599 notifications of chickenpox reported compared with 1,795 in 2008 and, a rate of 10.8 notifications per 100,000 population. The highest rates were reported from the Northern Territory (87 notifications, 38.7 per 100,000 population) and South Australia (475, 29.3 per 100,000) reflecting the increased case ascertainment in these jurisdictions due to their practice of following up VZV notifications.
Sixty-four per cent of notifications (1,028) occurred in children aged less than 10 years. The highest rates were in the 5–9 years age group (627 notifications, 46.2 per 100,000 population; Figure 62). In 2009, the rate for children aged less than 4 years (28.2 per 100,000) was approximately half of the 2008 rate (59.0 per 100,000).
Figure 62: Notification rate for chickenpox, Australia,* 2009, by age group and sex
* Excluding New South Wales.
Indigenous status was recorded for 98% (1,569) of notifications, the majority of which 82% (1,305) were non-Indigenous.
Of the 1,599 notifications for chickenpox, information on vaccination was available for 30% (543/1,790) and 80% (432/543) of these were unvaccinated.
Shingles occurs most commonly with increasing age (> 50 years), impaired immunity, and a history of chickenpox in the first year of life. Reactivation of VZV causing shingles is thought to be due to a decline in cellular immunity to the virus, and in the majority of cases presents clinically as a unilateral vesicular rash in a dermatomal distribution. Associated symptoms may include headache, photophobia, malaise, and an 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 pain or post-herpetic neuralgia.21
There were 2,659 notifications of shingles reported to NNDSS in 2009, an increase when compared with 2,309 in 2008, and a rate of 18.0 notifications per 100,000 population. The highest rates were in South Australia (1,045, 64.4 per 100,000) and the Northern Territory (112, 49.8 per 100,000).
There were more female notifications (1,470; 55.3%) than males (1,187; 44.7%), which was similar to 2008. The highest rates were in the 85 years or over age group (126, 32.9 per 100,000; Figure 63).
Figure 63: Notification rate for shingles, Australia,* 2009, by age group and sex
* Excluding New South Wales.
Indigenous status was recorded for 81% (2,166) of notifications, the majority of which 97%, (2,102/2,166) were non-Indigenous.
This issue - Vol 35 No 2, June 2011
NNDSS Annual report 2009