This extract of the NNDSS annual report 2010 was published in Communicable Diseases Intelligence Vol 36 No 1 March 2012. A print friendly full version may be downloaded as a PDF 1862 KB.
The full issue of CDI is available as a PDF file (2586 KB) or by individual articles from this issue's table of contents
Vaccine preventable diseases
This section summarises the national notification surveillance data for notifiable diseases targeted by the National Immunisation Program (NIP) in 2010. These include diphtheria, invasive Haemophilus influenzae type b infection, laboratory-confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease, poliomyelitis, rubella, tetanus and varicella zoster infections (chickenpox, shingles and unspecified). Data on hepatitis B and invasive meningococcal disease, which are also targeted by the NIP, can be found in this report under ‘Bloodborne diseases’ and ‘Other bacterial infections’ respectively. Other vaccine preventable diseases (VPDs) presented in this report include hepatitis A and Q fever under the ‘Gastrointestinal’ and ‘Zoonoses’ sections respectively. For more 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 was published as the December 2010 supplement issue of CDI. 42
In 2010, there were 61,964 notified cases of VPDs, representing 30% of all notified cases to NNDSS and a 39% decrease compared with 2009 (n = 102,003). Pertussis was the most commonly notified VPD (n = 34,793, 56% of the total), reflecting the ongoing epidemic of this disease in 2010, followed by influenza (n = 13,419, 22%). The number of notifications and notification rates for VPDs in Australia are shown in Tables 2 and 3.
Whilst there were no new vaccines added to the NIP in 2010, eligibility for the seasonal trivalent influenza vaccine, which included the pandemic (H1N1) 2009 strain was extended to protect a wider range of vulnerable people. Those eligible for the seasonal influenza vaccine under the NIP in 2010 included individuals with medical conditions predisposing them to severe influenza, Aboriginal and Torres Strait Islander people aged 15 years and over, pregnant women, and persons aged 65 years or over. The seasonal influenza vaccine was also available to the rest of the population if they wished to pay for a prescription or were able to obtain the vaccine through workplace or other programs. In addition, the monovalent vaccine developed in response to the 2009 influenza pandemic continued to be available for free to everyone not eligible for the free seasonal vaccine and was distributed through the national Pandemic (H1N1) 2009 Vaccination Program.
Vaccination coverage is an important factor influencing the incidence of vaccine preventable diseases. Since the commencement of the Australian Childhood Immunisation Register in 1996, immunisation coverage in children has been high by international standards, although geographical pockets of lower coverage remain, in which there is an increased potential for VPDs to occur and circulate. These areas 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 can be much higher.43
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 for recording ‘vaccine type’ and ‘vaccination date’ for each dose. The new fields were intended to replace the old fields, with a transition period allowing either field to be utilised. In 2010, 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 provided by the states and territories 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.
Diphtheria is an acute toxin-mediated systemic disease caused by the bacterium Corynebacterium diphtheriae. Infection is usually localised to the skin (cutaneous diphtheria) or to the throat (pharyngeal diphtheria), in which a membranous inflammation of the upper respiratory tract can cause airway obstruction. Systemic complications caused by the bacteria’s exotoxin can occur in both pharyngeal and cutaneous diphtheria. Diphtheria is spread by respiratory droplets or by direct contact with skin lesions or articles soiled by infected individuals.16 While there are non-toxigenic strains of C. diphtheriae, they usually only cause mild throat or skin infection and are not nationally notifiable. In Australia, serosurveillance data indicate that childhood immunity to diphtheria is greater than 99% however, waning immunity amongst adults may result in this population being susceptible with the most likely source of exposure being through overseas travel to countries where diphtheria remains endemic.44
There were no notified cases of diphtheria reported to NNDSS in 2010. The last case of diphtheria reported in Australia was a case of cutaneous diphtheria in 2001, the only case reported since 1992.
Influenza is a viral respiratory infection that causes annual epidemics of respiratory disease. In temperate climates there is usually an increase in influenza transmission during the winter months, from May to October, with the intensity and severity of a season varying from year to year. As only laboratory confirmed cases of influenza are notifiable, it can be difficult to draw conclusions about the true level of influenza activity in the community, due to an unknown proportion of cases where no health care was sought, or no testing performed.
Notifications of influenza decreased substantially in 2010 following the 2009 pandemic year. The 2010 influenza season in Australia was relatively mild, with notification levels comparable to pre-pandemic years. There were 13,419 notified cases of laboratory-confirmed influenza reported to NNDSS in 2010, which was less than a quarter of the number of cases from the previous year. The season peaked in September with 4,944 cases for the month, which was later than in previous years (Figure 30). Higher than usual levels of influenza activity continued across the summer months following the end of the influenza season, and into the following year.
Figure 30: Notified cases of laboratory-confirmed influenza, Australia, 2005 to 2010, by month and year
Notification rates were highest in South Australia (258 per 100,000), followed by the Northern Territory (209 per 100,000), with a large gap to the next highest notification rates in Queensland and Western Australian (both 71 per 100,000). Notifications in these jurisdictions were all higher than the national notification rate of 60 per 100,000. Queensland consistently had the highest number of notifications in previous years. In 2010, South Australia replaced Queensland as the jurisdiction with the highest proportion of influenza cases notified (32%), it is thought this increase was due to an actual increase in influenza activity and not an artefact of testing practices (Figure 31).
Figure 31: Notified cases of laboratory-confirmed influenza, Australia, 2010, by week and state or territory
Females accounted for 7,034 (52%) of the 13,419 influenza notifications in 2010. Notifications were higher amongst females than males in most age groups except in the age groups less than 15 years where this was reversed (Figure 32). This likely reflects the health seeking behaviour of adult females, as they tend to account for a greater proportion of encounters in general practice.45 The highest number of influenza notifications occurred in the 0–4 year age group in both males and females; together they accounted for 12% of all notifications. Over half of the notifications were in people aged less than 30 years.
Figure 32: Notified cases of laboratory-confirmed influenza, Australia, 2010, by age group* and sex
* Excludes 96 notifications for whom age or sex were not reported.
Notification rates were highest in the 0–4 year age group (109 notifications per 100,000) with a secondary peak seen in those aged 25–29 years (75 per 100,000), however overall notification rates of influenza decreased with increasing age (Figure 33). Although notifications in 2010 were predominantly the pandemic (H1N1) 2009 strain, the age distribution profile was quite different in the younger age groups in 2010 compared with 2009. In 2009 the highest rates were seen in the 5–9, 10–14 and 15–19 year age groups, with rates in those over 30 years substantially declining relative to the younger age groups. In pre-pandemic seasons, there was typically an increase of notification rates in those aged 70 years and over compared with other adults, this pattern was not observed in 2009 or in 2010 (Figure 33).
Figure 33: Rate for laboratory-confirmed influenza, Australia, 2006 to 2010, by age and year
In 2010, almost all (n = 13,402) of the influenza notifications in NNDSS had some level of influenza typing reported. Of those with type information, 90% (n = 12,050) were type A (56% were pandemic (H1N1) 2009, 30% were A (not subtyped) and 4% were A(H3N2)) and 10% (n = 1,301) were type B. Mixed influenza type A and B infections accounted for less than 1% of notifications and typing data were not available for 17 cases (Figure 34).
Figure 34: Notified cases of laboratory-confirmed influenza, Australia, 2010, by week and subtype
In 2010, 1,908 Australian influenza viruses were typed and subtyped by the WHO Collaborating Centre for Reference and Research on Influenza (WHOCC). This represented 14% of laboratory-confirmed cases reported to the NNDSS. Pandemic (H1N1) 2009 represented the majority (75%) of viruses, followed by influenza B (14%) and influenza A(H3N2) (11%). Pandemic (H1N1) 2009 replaced previous seasonal A(H1N1) viruses in 2010.
The WHOCC conducted antigenic characterisation on 1,543 of the influenza virus isolates. The vast majority of pandemic (H1N1) 2009 isolates were characterised as A/California/7/2009-like. Of the circulating influenza A(H3N2) viruses analysed, most were antigenically similar to the A/Perth/16/2009 virus. Most influenza B viruses detected, were closely related to the B/Brisbane/60/2008 virus.
* Notifications of influenza ‘untyped’ (n = 17) and type A and B (n = 51) were excluded from analysis.
All 3 strains of 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), an A/Perth/16/2009 (H3N2)-like virus and B/Brisbane/60/2008 (a representative of the B/Victoria/2/87 lineage). Almost all the circulating viruses that were isolated in 2010 were antigenically similar to the 2010 vaccine viruses.46
In 2010, the WHOCC conducted antiviral susceptibility testing on 1,320 influenza viruses for resistance to the antiviral drugs oseltamivir and zanamivir. Neuraminidase inhibition assay was performed on 1,277 viral isolates. Four of the pandemic (H1N1) 2009 isolates tested showed resistance to oseltamirvir due to the H275Y neuraminidase mutation. Pyrosequencing of 43 pandemic (H1N1) 2009 clinical specimens found 2 specimens with the same H275Y mutation, which is known to confer oseltamivir resistance. Therefore a total of 6 influenza viruses showed oseltamivir resistance but none were resistant to zanamivir. No oseltamivir or zanamivir resistance was detected in any of the A(H3N2) or influenza B viruses.
Invasive Haemophilus influenzae type b disease
Invasive Haemophilus influenzae type b (Hib) 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 notified cases in Australia (Figure 35), which now has one of the lowest rates of Hib in the world.42
Figure 35: Notified cases and rate for invasive Haemophilus influenzae type b infection, Australia, 1991 to 2010, by year
There were 24 notified cases of Hib disease in 2010; a rate of 0.1 per 100,000 population and five more than reported in 2009. The majority of cases (n = 10) were in children aged less than 5 years who had the highest rate of notification (0.7 per 100,000 population), and 60% (n = 6) of which were infants less than one year including 1 case in an infant less than 6 months of age. There were no cases in persons between the ages of 6 and 22 years. The remaining 13 cases ranged in age between 23 and 100 years, and included 4 cases in the 50–54 year age group (Figure 36). The majority, 63% (n = 15) of cases were female, predominately in age groups over 4 years.
Indigenous status was complete for 92% (n = 22) of Hib cases in 2010. Thirty-six per cent (8/22) were reported as Indigenous. The rate for Hib in 2010 was 1.4 in Indigenous people and 0.07 in non-Indigenous people, giving a rate ratio of 20:1. Rates of Hib infection in the Indigenous population fluctuated between 2005 and 2010 from 0.6 to 1.4 and represented a 5– to 27-fold increase compared with rates in the non-Indigenous population. The wide variation in rates was due to the low number of cases. Indigenous status recorded as unknown or missing represented an average of 1.5 cases between 2005 and 2010 and were included in the non-Indigenous category for the purpose of this analysis.
Figure 36: Rate for invasive Haemophilus influenzae type b infection, Australia, 2010, by age group and sex
In 2010, all children under the age of 18 years were eligible for Hib vaccination in infancy. Hib vaccine was introduced to the NIP in April 1993 for all children born after February 1993. Vaccination status was known for all 10 cases in children aged less than 5 years of which 9 were fully vaccinated for age and 1 was unvaccinated. Of the 9 vaccinated cases, 5 had received all recommended doses of Hib containing vaccine under the NIP.
Invasive pneumococcal disease
There were 1,644 notified cases of invasive pneumococcal disease (IPD) in Australia in 2010; a rate of 7.4 per 100,000 population. This was an increase of 6% from the 1,557 reported in 2009 (7.1 per 100,000). An increase in rates in 2010, compared with 2009, was seen in New South Wales (6.9 per 100,000, n = 503) Queensland (6.0 per 100,000, n = 271), Tasmania (9.1 per 100,000, n = 46), Victoria (7.3 per 100,000, 406 cases) and Western Australia (8.6 per 100,000, 198 cases). A decrease in rates was noted in the Australian Capital Territory (6.7 per 100,000, n = 24), the Northern Territory (24 per 100,000, n = 56) and South Australia (8.5 per 100,000, n = 140).
In 2010, males accounted for 56% (914 per 100,000) of the 1,644 notified cases of IPD. In most age groups there were more males than females, resulting in a male to female ratio of 1.3:1. Figure 37 shows that the highest rates of IPD in 2010 were for persons aged 85 years or over (34 per 100,000) and in children aged 1 year (33 per 100,000).
Figure 37: Rate for invasive pneumococcal disease, Australia, 2010, by age group and sex
In Australia, pneumococcal vaccination is recommended as part of routine immunisation for children, older Australians and Aboriginal and Torres Strait Islander people. The 7vPCV vaccine was added to the NIP schedule for Indigenous and medically at-risk children in 2001 and for all children up to 2 years of age from January 2005.11 National pre-vaccination data are not available for the Indigenous population, however since surveillance began in 2002 the rate of disease due to disease caused by serotypes covered by 7vPCV in Indigenous children, aged less than 5 years, decreased from 35 per 100,000 to 1.4 per 100,000 in 2010 (Figure 38). In non-Indigenous children aged less than 5 years, the rates of IPD disease caused by serotypes covered by 7vPCV decreased since the introduction of the vaccine on the NIP in 2005, with a rate of 0.9 per 100,000 reported in 2010. Rates of disease caused by non-7vPCV serotypes over the same period increased for both Indigenous and non-Indigenous children, this included a 5-fold increase in the number of cases due to serotype 19A in non-Indigenous children over the period. The substantial increases in 19A serotype disease seen in non-Indigenous children were not evident in Indigenous children.
Figure 38: Rate for invasive pneumococcal disease in children aged less than 5 years, 2002 to 2010, by Indigenous status and year
7vPCV Disease caused by serotypes not covered by the vaccine.
Non-7vPCV Disease cause by serotypes not covered by the vaccine.
Overall, rates of IPD disease caused serotypes covered by 7vPCV declined between 2004 and 2010 from 7.7 per 100,000 to 0.7 per 100,000 (1,549 to 149 cases). The decline is seen across all age groups (Figure 39).
Figure 39: Rate for invasive pneumococcal disease caused by 7vPCV serotypes, Australia, 2002 to 2010, by age group and year
Enhanced data were collected on cases of IPD in all Australian jurisdictions during 2010. 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 2–4 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,16 which is always fatal.11 Evidence suggests that endemic measles has been eliminated from Australia, since at least 2005.47
There were 70 notified cases of measles reported to NNDSS in 2010 representing a rate of 0.3 per 100,000 population. Cases were reported from all states and territories with the exclusion of Tasmania. The majority of cases (n = 25) occurred in New South Wales, followed by Victoria (n = 15), Queensland (n = 14), Western Australia (n = 11), the Northern Territory (n = 2), South Australia (n = 2) and the Australian Capital Territory (n = 1). There were no cases in Tasmania (Figure 40).
Figure 40: Notified cases of measles, Australia, 2005 to 2010, by month and year and state or territory
In 2010, cases were evenly distributed by sex. Age at diagnosis ranged from 1 to 62 years with a median of 23 years and there were no cases amongst infants less than 1 year. The majority of cases (n = 50) were between 10 and 34 years of age. However, 4 cases were amongst those born before 1968, a cohort that is considered to have high levels of natural immunity48 (Figure 41).
Figure 41: Rate for measles, Australia, 2010, by age group and sex
Between 2005 and 2010 there were 386 notified cases, 93% (n = 369) of which were less than 40 years of age. During this 5-year period, rates were highest amongst those less than 5 years of age (0.8 per 100,000 population) followed closely by those in the 10–14 (0.7) and the 25–29 (0.6) year age groups (Figure 42).
Figure 42: Rate for measles, Australia, 2005 to 2010 combined, by age group
In 2010, 46% (n = 32) of notified cases were reported as being acquired from overseas including: South Africa (n = 6), Indonesia (n = 4), France (n = 3), Vietnam (n = 3), Cambodia (n = 2) and 1 importation each from China, Germany, Italy, Malawi, Malaysia, New Zealand, Pakistan, the Philippines, Singapore, Sri Lanka, Thailand, the United Kingdom, France and South Africa. Of the 38 locally-acquired cases, 36 were epidemiologically linked to an imported case in 8 separate clusters and the remaining two were part of a locally-acquired cluster in Victoria, for which the original source of infection could not be determined. There were 9 clusters during 2010, the largest of which occurred in the Tweed River region of New South Wales (n = 14), in an area of low vaccination coverage. Genotyping was available for each cluster with D9 the most common serotype (Figure 43).
Figure 43: Measles clusters, Australia, 2010, by state or territory, genotype and importation status
Two doses of the measles–mumps-rubella vaccine (MMR) are funded under the NIP for children 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 second dose.11
Sixty-four of the 70 cases notified in 2010 were born after 31 December 1969 and therefore eligible for a publicly funded measles-containing vaccine. Of the 5 cases aged between 1 and 3 years of age who were eligible for 1 dose of a measles-containing vaccine, one was fully vaccinated for age, three were not vaccinated and one was of unknown vaccination status. Of the remaining 59 cases, who were aged 4 years or older and eligible for 2 doses, the majority (n = 31) were not vaccinated, nine were partially vaccinated for age, 5 were fully vaccinated for age and 14 were of unknown 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. The characteristic bilateral, or occasionally unilateral, parotid swelling occurs in 60%–70% of clinical cases, however a high proportion have non-specific symptoms including fever, headache, malaise, myalgia and anorexia, with approximately one-third of infections being asymptomatic.16 Mumps is a multi-system infection, with 30% of post-pubertal males experiencing epididymo-orchitis.49
In 2010, there were 95 notified cases of mumps; a rate of 0.4 per 100,000 population, compared with the 165 cases and a rate of 0.7 per 100,000 reported in 2009. The number of notified cases has continued to decrease nationally since reaching a peak in 2007. Cases in 2010 were reported from all jurisdictions except Tasmania, with 40% (n = 38) occurring in New South Wales followed by 27% (n = 26) in Queensland (Figure 44). The highest rate was in the Northern Territory with 2 reported cases (0.9 per 100,000) followed by Western Australia (0.7 per 100,000) with 15 cases reported in 2010.
Figure 44: Notified cases of mumps, Australia, 2005 to 2010, by month and year and state or territory
In 2010, cases of mumps were notified across all age groups with the majority (n = 45) occurring amongst young adults between the ages of 25 and 44 years, reflecting historical vaccination schedules (Figure 45). Sixty-two per cent of cases were in females; a higher proportion than in the past 5 years and giving a male to female rate ratio of 0.6:1. The highest rates for females occurred in the 25–29, 30–34 and 40–44 year age groups respectively, while for males rates were highest in the 40–44 year age group followed by the 35–39 year age group.
Figure 45: Rate for mumps, Australia, 2010, by age group and sex
Rates in all age groups have continued to decline in 2010 (Figure 46).
Figure 46: Rate for mumps, Australia, 2005 to 2010, by year and age group
Indigenous status was reported for 50% of mumps cases, of which 4% (n = 2) were reported as Indigenous. In 2009, 10% (n = 11) of cases were reported as Indigenous.
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 first and second dose respectively.50,51 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.51
The mumps vaccine was first available in Australia in 1981 with people born after that eligible for 2 doses of a mumps-containing vaccine.52 In 2010, there were 37 notified cases in individuals born after 31 December 1980. Of these, none were less than 1 year of age, two were aged between 1 and 3 years and eligible for 1 dose and were fully vaccinated for age. The majority of cases (35/37) were aged 4 years or older. Of these, 17% (n = 6) were fully vaccinated for age, 6% (n = 2) were partially vaccinated for age, 11% (n = 4) unvaccinated and the majority, (66%) were of unknown vaccination status.
Pertussis was the most commonly notified vaccine preventable illness in Australia in 2010. It is a highly infectious disease caused by Bordetella pertussis and is 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.53 In vaccinated populations these outbreaks tend to be smaller with less mortality and morbidity than in unvaccinated populations.16 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 at least the second vaccine dose at 4 months of age.54 The majority of notifications usually occur in the spring and summer months.
In 2010 there continued to be large numbers of notified cases of pertussis associated with the Australia-wide epidemic which began in mid-2008 (Figure 47). The causes of this epidemic are likely to be multi-factorial with contributing factors including waning immunity levels in the vaccinated population in addition to improved testing methods and better case ascertainment.
Figure 47: Notified cases of pertussis, Australia, 2005 to 2010, by month and year and state or territory
In 2009, the Australian Technical Advisory Group on Immunisation (ATAGI) convened a Pertussis Working Party to consider the use of the combined diphtheriatetanuspertussis (DTPa) vaccine in young children, and the duration of effectiveness of the diphtheriatetanuspertussis (dTpa) vaccine in adolescents/adults. On the basis of evidence provided by the working party, ATAGI endorsed recommendations that the first dose of the pertussis-containing vaccine could be brought forward from 8 weeks to 6 weeks,55 the scheduled fourth dose of vaccine could be administered from the age of 3 years and 6 months, and that the adolescent booster dose could be given from 11 to 13 years of age to better protect siblings, especially newborns.56 States and territories continued to provide ongoing public awareness campaigns and most extended funding during 2010 for booster vaccination programs for parents and carers of infants, as part of a cocooning strategy to protect vulnerable infants from infection.
There were 34,793 notified cases of pertussis; a rate of 156 per 100,000 and 2.5 times the 5-year mean. Notifications included 3 pertussis related deaths Two of the deaths were recorded amongst infants less than 2 months of age and too young to be protected by vaccination, while the third death was a person 70 years of age.
In 2010, pertussis rates varied considerably by state or territory and residential location. Rates were highest in South Australia (449 per 100,000; n = 7,388) followed by the Australian Capital Territory (198 per 100,000; n = 712) and Queensland (182 per 100,000; n = 8,216) (Figure 48). Rates by SD varied widely across most jurisdictions except for South Australia where they were uniformly high (Map 3).
Figure 48: Rate for pertussis, Australia, 2007 to 2010, by year and state or territory
Map 3: Rates and counts* for pertussis, Australia, 2010, by Statistical Division and Statistical Subdivision of residence in the Northern Territory
* Numbers in the shaded Statistical Divisions and Statistical Subdivisions represent the count of notifications.
Note that rates by Statistical Division should be interpreted with caution as they can be high or low depending on the size of the population.
The timing of epidemic activity has varied across states and territories with the Northern Territory experiencing its peak rate in 2008 (217 per 100,000; n = 478), New South Wales (175 per 100,000; n = 12,448) and Tasmania (123 per 100,000; n = 618) in 2009 and Australian Capital Territory, Queensland, South Australia, Victoria and Western Australia in 2010 (Figure 48).
In 2010, females accounted for 57% (n = 19,950) of notifications, resulting in a male to female ratio of 0.7:1. Sixty cases had no sex specified. Females had higher rates in all age groups compared with males, except in the 85 years or over age group. Notification rates in 2010 varied widely with age. Children aged less than 15 years had a higher rate (321 per 100,000) than those adolescents and adults 15 years of age or over (117 per 100,000), with a rate ratio of 2.7 and consistent with the rate ratios in 2008 (2.2) and 2009 (2.6). The current epidemic trend of higher rates in children compared with adults is in contrast to the pre-epidemic years in which adults had a higher rate relative to children (rate ratios of 0.7, 0.3 and 0.5 respectively for 2005, 2006 and 2007). The highest rate amongst both males and females occurred in the 5–9 year age group (393 and 450 per 100,000 respectively) (Figure 49).
Figure 49: Rate for pertussis, Australia, 2010, by age group and sex
In 2010, rates amongst children in the 5–9 year age group (422 per 100,000) overtook infants aged less than 1 year (317 per 100,000) to have the highest rate for the first time since 2005 (except for 2006 in which adults 60 years or over had the highest rate and infants the second highest).
Between 2005 and 2007, a period inclusive of the last national epidemic in 2005/2006, age group rates either declined or remained relatively constant. Since 2007, rates have been increasing most markedly amongst those less than 15 years of age. In 2010 rates continued to increase all age groups, especially the 5–9 and 10–14 year age groups, compared with 2009, except those less than 5 years of age (Figure 50).
Figure 50: Rate for pertussis, Australia, 2005 to 2010, by year and age group
While the pertussis vaccine is not 100% effective and does not confer life-long immunity, vaccine effectiveness amongst Australian children has been estimated to range from 82% to 89% with the lower figure representing the cohort of children who would not have been eligible for the 18 month booster dose, which was removed from the NIP in 2003.57 Immunity to the disease decreases over time post-vaccination with estimates of protection remaining for 4–12 years.58 The current vaccine schedule for pertussis under the NIP includes a dose provided at 2, 4 and 6 months of age followed by a booster at 4 years of age and again at 12–17 years of age (the timing of this last booster dose varies by jurisdiction). In response to the ongoing epidemic in 2010, some infants were being provided their first vaccination at 6 weeks of age and their fourth from 3.5 years.
Follow-up is required in order to determine the vaccination status of individual cases. In a large outbreak follow-up of all cases is not possible and as per national guidelines jurisdictions prioritised follow-up for those less than 5 years of age. This age group made up 10% (n = 3,400) of all notified cases in 2010.
Information on vaccination status was available for 89% (3,030/3,400) of all cases in children less than 5 years of age of which 64% (1,944/3,030) were fully vaccinated for age, 15% (447 per 100,000) were partially vaccinated for age and 13% (379 per 100,000) were not vaccinated. Eight per cent (260 per 100,000) of cases were less than 6 weeks of age and therefore too young to be vaccinated.
Poliomyelitis is a highly infectious disease caused by gastrointestinal infection by poliovirus. Transmission occurs primarily person-to-person via the faecal-oral route. In most cases poliovirus infection is not symptomatic however in less than 1% of cases the virus may invade the nervous system and cause acute flaccid paralysis (AFP).16
In 2010 there were no notified cases of poliomyelitis in Australia, which along with the Western Pacific Region remained poliomyelitis free. Poliomyelitis is a notifiable disease in Australia with clinical and laboratory investigation conducted for cases involving patients of any age with a clinical suspicion of poliomyelitis. Australia follows the WHO protocol for poliomyelitis surveillance and focuses on investigating cases of AFP in children under 15 years of age. The WHO target for AFP surveillance in a polio non-endemic country is 1 case of AFP per 100,000 children aged less than 15 years, which in 2010, Australia achieved for the fourth consecutive year. More details can be found in the annual report of the Australian National Polio Reference Laboratory published in the CDI. A revised national polio case definition was endorsed by CDNA in 2010 and implemented on 1 July 2011. This revised definition is available on the Department of Health and Ageing’s web site at http://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-nndss-casedefs-cd_polio.htm. The principal changes were:
- the WHO definition of AFP was adopted under clinical definitive evidence;
- the laboratory definitive evidence was updated to include vaccine derived poliovirus; and
- a new section was added to include non-paralytic cases of poliovirus infection.
Rubella is generally a mild and self-limiting viral infectious disease. It is spread person-to-person through contact with respiratory secretions directly or via air-borne droplets. Clinically, rubella can be difficult to distinguish from other diseases which cause a febrile rash, such as measles, and is asymptomatic in up to 50% of cases. Rubella infection in pregnancy can result in foetal infection resulting in congenital rubella syndrome (CRS). CRS occurs in up to 90% of infants born to women who are infected during the first 10 weeks of pregnancy and may result in foetal malformations and death.16
In 2010, there were 44 notified cases of rubella; a rate of 0.2 per 100,000 population and an increase compared with the 27 notifications in 2009. The increase in cases in 2010 was not associated with any particular outbreak and was likely due to the sporadic nature and overall small number of cases reported annually. Notifications were reported from Victoria (n = 22), New South Wales (n = 13), Queensland (n = 5), Western Australia (n = 3) and the Australian Capital Territory (n = 1). The male to female ratio of notified cases in 2010 was 1.9:1, (29 males and 15 females). The majority (87%) of female cases were notified in women of child-bearing age (15–44 years of age). The majority (86%) of cases were adults aged between 20 and 49 years with a median age of 29.5 years (Figure 51). There were no notified cases of CRS reported in 2010.
Figure 51: Rate for rubella, Australia, 2010, by age group and sex
Rubella cases across the age groups have continued to trend at low levels since 2004, except for a spike amongst the 25–34 year age group in 2006 (Figure 52). This spike was primarily due to an increase in cases from South Eastern and Central Sydney, New South Wales for which no single source was identified.59
Figure 52: Rate of rubella, Australia, 2005 to 2010, by year and 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.11 Rubella vaccine is included in the combined MMR vaccine and provided under the NIP schedule at 12 months and 4 years of age.
Information on vaccination was available for 25% (n = 11) of rubella cases of which the majority, 73% (n = 8), were not vaccinated, two were reported as fully vaccinated for age and one was too young for routine vaccination.
Indigenous status was recorded for the majority (91%) of cases, all of whom were non-Indigenous.
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.16 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.11
Tetanus vaccination stimulates the production of antitoxin, which protects against the toxin produced by the organism. Complete immunisation (3 primary doses and 2 boosters included for children on the NIP) induces protective levels of antitoxin lasting throughout childhood but by middle age, about 50% of vaccinees have low or undetectable levels of immunity. It is recommended, though not funded under the NIP, that all adults who reach 50 years of age and have not received a booster of a tetanus-containing vaccine in the previous 10 years should have one.11
In 2010, there were 2 notified cases of tetanus, 1 male from New South Wales and 1 female from Victoria, both greater than 78 years of age. Neither case had vaccination status recorded.
Varicella zoster virus infections
The varicella zoster virus (VZV) is a highly contagious member of the herpesvirus family and causes two distinct illnesses: chickenpox (or varicella) following initial infection and shingles (or herpes zoster), which occurs following re-activation of latent virus in approximately 20%–30% of cases, most commonly after 50 years of age.16
In 2006, CDNA agreed to make 3 categories of VZV infection notifiable: chickenpox, shingles and varicella infection unspecified. With the exception of New South Wales, where VZV is not notifiable, 2010 was the second complete year in which all jurisdictions sent VZV data to NNDSS.
In 2010, there were 11,873 VZV notified cases from the 7 reporting jurisdictions. This was 6% more than in 2009. Sixty per cent (n = 7,152) were reported as unspecified varicella infection, 25% (n = 2,978) as shingles and 15% (n = 1,743) as chickenpox.
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 53), VZV unspecified accounted for 60% of all VZV notified cases in 2010, a decrease compared with 62% of the total in 2009.
There were 7,152 notified cases of unspecified VZV infections based on laboratory diagnoses compared with 6,977 in 2009 and a rate of 47 per 100,000 population The high proportion of unspecified VZV infection compared to 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 rate was reported from Queensland (86 per 100,000; n = 3,894), followed by Western Australia (38 per 100,000; n = 877) and Victoria (34 per 100,000; n = 1,912).The age and sex distribution of unspecified VZV is shown in Figure 54.
Figure 53: Proportion of notified cases for varicella zoster virus unspecified, chickenpox and shingles, 2010, by state or territory*
* Excluding New South Wales
Figure 54: Rate for varicella zoster virus infection (unspecified), Australia,* 2010, 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.11
In 2010, there were a total of 1,743 notified cases of chickenpox reported to NNDSS; a rate of 12 per 100,000, compared with 1,599 in 2009. The highest rate was reported from the Northern Territory (37 per 100,000; n = 84) and South Australia (23 per 100,000; n = 379) reflecting the increased case ascertainment in these jurisdictions compared with others.
The male female ratio in 2010 was 1:1 with males and females being fairly consistently represented across the age groups. Seventy per cent of cases (n = 1,212) occurred in children aged less than 10 years. The highest notification rates amongst both sexes and all age groups were amongst the 5–9 year age group (53 per 100,000; n = 725) (Figure 55). Although higher rates amongst children compared with adults is expected, they are likely to be biased by the jurisdictional practice of not following up adult cases.
Figure 55: Rate for chickenpox, Australia,* 2010, by age group and sex
* Excluding New South Wales.
Indigenous status was recorded for 89% (n = 1,552) of cases. Of these, 93% (n = 1,447) were non-Indigenous.
In November 2005, the varicella zoster vaccine was added to the NIP Schedule as a single dose due at 18 months of age (for children born on or after 1 May 2004), or as a catch-up dose at 10–13 years of age. In 2010, children born in 2004 and eligible for the 18-month dose would be 6 years of age or younger and as follow-up of cases does not routinely occur in those older than 7 years, analysis of vaccination status is restricted to this cohort. Of the 823 children less than 7 years of age, vaccination information was available for 77% (636/823) of cases of whom 44% (n = 277) were vaccinated, 16% (n = 102) were unvaccinated and 40% (n = 257) were aged less than 18 months and therefore ineligible for vaccination.
Shingles occurs most commonly with increasing age, impaired immunity, and a history of chickenpox in the first year of life. Reactivation of VZV causing shingles is thought to be due to a decline in cellular immunity to the virus, and in the majority of cases presents clinically as a unilateral vesicular rash in a dermatomal distribution. Associated symptoms may include headache, photophobia, malaise, and 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.16
There were 2,978 notified cases of shingles reported in 2010, a rate of 20 per 100,000 and a 10% increase compared with 2009. The highest rate was in South Australia (71 per 100,000; n = 1,166) followed by the Northern Territory (57 per 100,000; n = 130), reflecting the increased case ascertainment in these jurisdictions compared with others.
There were more female cases (n = 1,670) than males (n = 1,305); a ratio of 0.8:1. As expected, rates increased with age with the highest rate amongst those over 85 years of age or older (61 per 100,000; n = 159) (Figure 56).
Figure 56: Rate for shingles, Australia,* 2010, by age group and sex
* Excluding New South Wales.
Indigenous status was recorded for 87% (n = 2,579) of notified cases, of whom 97% (n = 2,489) were non-Indigenous.
Communicable Diseases Surveillance
This issue - Vol 36 No 1, March 2012
NNDSS Annual report 2010