Results - Part 5
Vaccine preventable diseases
This section summarises the national surveillance data for notifiable diseases targeted by the National Immunisation Program (NIP) in 2014. These include diphtheria, invasive Haemophilus influenzae type b (Hib) infection, laboratory confirmed influenza, measles, mumps, pertussis, invasive pneumococcal disease (IPD), poliomyelitis, rubella, tetanus and varicella zoster virus (VZV) infections (unspecified, chickenpox and shingles). Data on hepatitis B and invasive meningococcal disease, which are also targeted by the NIP, can be found in this report under ‘Bloodborne diseases’ and ‘Other bacterial infections’ respectively. Other vaccine preventable diseases (VPDs) presented in this report include hepatitis A and Q fever which can be found under the ‘Gastrointestinal’ and ‘Zoonoses’ sections respectively. For more detailed reports on historical data, including notifications, hospitalisations and deaths, readers are referred to the journal supplements ‘Vaccine Preventable Diseases in Australia’ and the ‘Australian Vaccine Preventable Diseases Epidemiological Review Series’ for additional analysis on individual diseases, which are published in CDI.
In 2014, there were 101,400 VPD notifications reported to the NNDSS, representing 37% of all reported cases and a 70% increase compared with 2013 (n=59,630). Influenza was the most commonly notified VPD with 67,742 cases (67%) reported, followed by pertussis (11,863, 12%). The number of notifications and notification rates for VPDs in Australia are shown in Table 4, Table 5 and Table 6.
Vaccination coverage is an important factor influencing the incidence of VPDs. Since the commencement of the Australian Childhood Immunisation Register in 1996, vaccination 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 still remain. As no vaccine is 100% effective, infections with these diseases sometimes do occur in fully vaccinated people. However, evidence shows vaccines do provide a substantially lower chance of developing infection or can reduce the severity of disease. 67–71
Information on a case’s vaccination history was previously recorded in the NNDSS using the ‘vaccination status’ field (fully or partially vaccinated for age or not vaccinated), plus fields capturing the number of doses, the last vaccination date and how the vaccination information was validated. In January 2008 new, more detailed fields were incorporated for recording ‘vaccine type’, and ‘vaccination date’ for each dose of vaccine given. The new fields were intended to replace the old fields, with a transition period allowing either field to be utilised. In 2014, all jurisdictions, except the Australian Capital Territory, were using the new 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 Handbook,32 and at least 14 days prior to disease onset.
Diphtheria is an acute pharyngeal or cutaneous infection caused mainly by toxigenic strains of Corynebacterium diphtheriae. The exotoxin acts locally on the mucous membranes of the respiratory tract, and on damaged skin, although this is not as common. Disease is mainly due to local membranous inflammation, which for pharyngeal diphtheria can cause airway obstruction. Occasionally, systemic infections occur and cause damage to the myocardium, nervous system and kidneys. Diphtheria is spread by respiratory droplets or direct contact with nasopharyngeal secretions or skin lesions. While there are non-toxigenic strains of C. diphtheriae, they usually only cause mild throat or skin infection and are not nationally notifiable.22
Epidemiological situation in 2014
In 2014, there were 2 notifications of diphtheria reported. Both cases were cutaneous, reported in Queensland and were imported from Tokelau and Cambodia. One case was reported as vaccinated and the other was of unknown vaccination status.
Diphtheria is rare in Australia, with most cases associated with sporadic importations from countries in which the disease remains endemic. From 2001 to 2013, there were 7 cases of diphtheria reported to the NNDSS, including 1 case in 2001, a cluster of 3 cases and a sporadic case in 2011 and 2 cases in 2013. Of these, 5 were imported and 2 were linked to an imported case.
The seasonal increase in laboratory confirmed influenza notifications for 2014 was slightly earlier and reached a higher peak than recent years, excluding the 2009 influenza pandemic.
Nationally, influenza A was the predominant influenza virus type. However, the distribution of influenza types and subtypes was variable between jurisdictions and changed as the season progressed. Unlike the rest of the country where influenza A(H1N1)pdm09 predominated throughout the season, New South Wales and the Australian Capital Territory saw influenza A(H3N2) circulating at higher levels.
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.72 The disease ranges from asymptomatic73 through to mild upper respiratory tract illness, to severe complications including pneumonia. The severity of disease is determined by features intrinsic to the virus including its similarity to previous circulating and vaccine strains and by host factors including the age, level of immunity and presence of chronic medical conditions.74,75
Annual influenza vaccination is the primary means of preventing or attenuating influenza and its complications and is included in the NIP for individuals who are at increased risk of complications from influenza infection. In 2014, the NIP funded influenza vaccination for people aged 6 months and over with medical conditions placing them at risk of serious complications due to influenza, Aboriginal and Torres Strait Islander people aged 15 years or over, pregnant women and people aged 65 years or over.32
Epidemiological situation in 2014
In 2014, there were 67,742 notifications of laboratory confirmed influenza, which was almost 2.4 times the number of notified cases reported in 2013 (n=28,311) (Figure 49). The number of notifications recorded in 2014 is the highest on record and was 21% higher than 2009 (n=56,026), the year of the last influenza pandemic.
Notification rates were highest in South Australia (655 per 100,000) and Queensland (380 per 100,000). Notifications rates in the Australian Capital Territory, New South Wales, and the Northern Territory were somewhat similar to the national notification rate of 289 per 100,000, while rates reported in Tasmania, Victoria and Western Australia were substantially lower than the national rate at 131, 170 and 205 per 100,000 respectively. New South Wales reported the highest number of influenza cases of any jurisdiction (n=20,877), comprising 31% of notifications nationally (Figure 50).
Age and sex distribution
The highest number of influenza notifications occurred in the 0–4 years and 5–9 years age groups (n=8,415 and 5,510, respectively), which together accounted for 21% of all notifications (Figure 51). Notification rates were highest in the 0–4 years and over 85 years age groups (551 and 547 notifications per 100,000 respectively) with an additional peak in the 35–39 years age group (312 notifications per 100,000) (Figure 51).
In seasons dominated by the influenza A(H1N1)pdm09 virus, such as 2009, 2010 and 2011, the age distribution of influenza notification rates showed a downward trend with increasing age (Figure 52). For comparison, in 2012, which was dominated by influenza A(H3N2), the age distribution of influenza notifications was bimodal with peaks in those aged under 10 years and in those aged 70 years or over. The 2014 influenza season was characterised by co-circulation of A(H1N1)pdm09 and influenza A(H3N2) with the proportion of influenza B viruses rising towards the end of the year. This broad strain distribution has seen the burden of disease carried across a breadth of age groups.
In 2014, females accounted for 54% (n=35,538) of the influenza notifications for which sex was reported. The age group-specific rate of influenza in males exceeded that in females in age groups less than 15 years and greater than 75 years.
Influenza notifications during the 2013–14 inter-seasonal period were the highest on record with an average of 1,358 notifications per month. It is unclear whether this was a reflection of a higher prevalence of influenza circulating in the community at this time, an increased rate of testing or another factor. Queensland reported the largest number of inter-seasonal influenza notifications.
The seasonal increase of influenza notifications in 2014 started in June, rose sharply and peaked in August. This was slightly earlier than the seasonal patterns in the past 3 influenza seasons (Figure 53). The peak was higher than previous years, excluding the 2009 influenza pandemic. The majority of jurisdictions peaked in activity around late August, followed by a steady decline in influenza activity back to inter-seasonal levels by November.
Nationally in 2014, Indigenous status was reported in 40% (n=27,052) of laboratory confirmed notifications of influenza. Indigenous status completeness was greater than 50% in 3 jurisdictions: the Northern Territory (100%), South Australia (87%) and Western Australia (93%). Among these, the combined notification rate for influenza in Indigenous peoples was 584 per 100,000 and 371 per 100,000 among non-Indigenous population, representing a notification rate ratio of 1.6.
Nationally, there were 132 influenza-associated deaths notified to the NNDSS, with a median age of 75 years (range 1–103 years). The majority of deaths were associated with influenza A infections (n=126; 95%), and of these, 93 were associated with influenza A(unsubtyped) infections, 24 were A(H1N1)pdm09 and 9 were A(H3N2). Indigenous status was reported for 81% (n=107) of the influenza-associated deaths; and Indigenous peoples accounted for 6% (n=6) of these deaths. The number of influenza-associated deaths reported to the NNDSS is reliant on the follow-up of cases to determine the outcome of their infection and most likely underestimates the true mortality associated with this disease.
National Notifiable Diseases Surveillance System
In 2014, typing data were reported for all but 18 laboratory confirmed influenza notifications. Of notifications with typing information, 88% were due to influenza type A (n=59,563) and 12% were due to influenza type B (n=8,052). Whilst the majority of notifications of influenza A were reported as unsubtyped (69%, n=46,771), influenza A(H1N1)pdm09 and influenza A(H3N2) circulated in similar proportions (10%, n=6,922 and 9%, n=5,870 respectively). Mixed influenza type A and B infections accounted for less than 1% of notifications (n=96). There were 13 notifications of influenza type C (Figure 54).
As in previous years, influenza A remained the predominant virus type in 2014 (Figure 55). Influenza A(H3N2) accounted for a larger burden of disease due to influenza A than has been seen in previous years, with the exception of 2012 where almost all disease due to influenza A was caused by influenza A(H3N2). Influenza B circulated at lower levels in 2014 when compared with the previous 3 years.
While influenza A(H1N1)pdm09 and influenza A(H3N2) circulated in similar proportions nationally, distribution varied between jurisdictions. Influenza A(H1N1)pdm09 predominated across most jurisdictions throughout the season. However, influenza A(H3N2) was predominant in New South Wales and the Australian Capital Territory, with late season increases noted in Queensland, Western Australia, the Northern Territory and Tasmania.
WHO Collaborating Centre for Reference and Research on Influenza
For 2014, the WHO Collaborating Centre for Reference and Research on Influenza (WHOCC) analysed 2,072 specimens from influenza cases identified in Australia. Specimens are submitted to the WHOCC from laboratories according to guidelines that aim for successful isolation of viruses and likelihood of obtaining a vaccine candidate. WHOCC specimens therefore do not constitute a representative sample of influenza infections, which most likely accounts for differences in virus subtype distribution between NNDSS and WHOCC.
The number of samples analysed by the WHOCC represented approximately 3% of the 67,742 laboratory confirmed cases reported to the NNDSS compared with 1,532 isolates in 2013 representing 5.4% of notifications. The majority of specimens were influenza A(H1N1)pdm09 (61%, n=1,263) with 27% influenza A(H3N2) (n=562) and 12% influenza B (n=247) (Figure 56). While the proportion of WHOCC isolates typed as influenza B was similar to that reported in laboratory confirmed notifications, the distribution of influenza A(H1N1)pdm09 and influenza A(H3N2) differed, assuming that the notifications to NNDSS of influenza A reported as unsubtyped were similarly distributed as the subtyped notifications.
Text version of Figure 56b (TXT 1 KB)
The WHOCC assessed the antigenic similarity of circulating influenza virus isolates to reference strains included in the trivalent vaccine from recent years using the haemagglutination inhibition assay. The 2014 seasonal influenza vaccine contained 2 changes from 2013 and included an A/Texas/50/2012 (H3N2)-like virus and a B/Massachusetts/2/2012-like virus.
The majority of the A(H1N1)pdm09 isolates (1,257 of 1,263) were antigenically similar to the A(H1N1) component of the influenza vaccine, which has been used each year since 2010. The remaining 6 (0.5%) isolates were characterised as ‘low reactors’. This suggests that the A(H1N1) viruses, which have been circulating since the 2009 pandemic continue to be genetically and antigenically stable. By comparison, approximately 6% (33/562) of A(H3N2) isolates were antigenically drifted from the A/Texas/50/2012 vaccine strain and, characterised as ‘low reactors’, the remainder of the A(H3N2) viruses were genetically distinct from A/Texas/50/2012.
Of the influenza B viruses tested (n=247), 83% (206) were from the B/Yamagata lineage, with the remainder from the B/Victoria lineage. A high proportion of B/Yamagata viruses (70%, 145/206) were low reactors to the B component of the 2014 vaccine (B/Massachusetts/2/2012-like) thus the vaccine was a poor match to the circulating lineages. Further studies determined that the majority (86%, 178/206) of B/Yamagata viruses circulating in 2014 were more antigenically similar to the 2013 trivalent influenza vaccine B component (B/Wisconsin/1/2010–like). B/Massachusetts/2/2012 and B/Wisconsin/1/2010 were both B/Yamagata viruses but sit within genetically-distinct clades in the influenza phylogenetic tree.
Viruses submitted to the WHOCC in 2014 were also tested for sensitivity to the neuraminidase inhibitor class of antiviral drugs. Neuraminidase inhibition assays were performed on 2,025 virus isolates consisting of 1,242 A(H1N1)pdm09, 551 A(H3N2) and 232 influenza B viruses. Reduced inhibition by oseltamivir was detected in 3 A(H1N1)pdm09 isolates and reduced inhibition by zanamivir was detected in a single A(H3N2) isolate. In recent years, resistance to oseltamivir in Australian-sourced isolates, has been mediated primarily through the well characterised H275Y mutation,76 however, this was not the case in 2014 where none of the resistant isolates carried this mutation.
Due to the circulation of drifted A(H3N2) viruses and the predominance of a different B/Yamagata-lineage in Australia and elsewhere in the Southern Hemisphere, there were 2 updates recommended for the 2015 trivalent influenza vaccine for Australia, with the incorporation of an A/Switzerland9715293/2013-like A(H3N2) virus and a B/Phuket/3073/2013-like B/Yamagata virus (the latter virus being isolated at the WHOCC) being added to the existing A/California/7/2009-like A(H1N1)pdm09 virus.
Enhanced surveillance datasets
In addition to NNDSS data, a series of targeted influenza surveillance systems operated during 2014. Together these systems collected data, which were used to describe the season with respect to epidemiology, morbidity, mortality and virology and supported the conclusions drawn from analyses of NNDSS notification data. Enhanced influenza surveillance was based on the following additional sources of data:
- the number and proportion of calls to a national health call centre network for influenza or influenza-like illness (ILI);
- rates of ILI from a community survey;
- consultation rates for ILI identified by sentinel general practitioners;
- consultation rates for ILI identified by hospital emergency departments in Western Australia, New South Wales and the Northern Territory;
- hospitalised cases of influenza from 17 sentinel hospitals (adult and paediatric) across Australia;
- mortality data from the New South Wales Registry of Births, Deaths and Marriages; and
- typing and subtyping for influenza from sentinel laboratories in New South Wales, Victoria, Western Australia and Tasmania.
These data sources were used to inform the overall picture of influenza activity in Australia and comprehensive analysis of these data are provided in the fortnightly Australian Influenza Surveillance Report, which was published during the season, and in the annual National Influenza Surveillance Scheme report.
In Australia, the 2014 influenza season was slightly earlier than in previous seasons with active transmission of influenza virus commencing in mid-June, sharply increasing in mid-July and peaking in mid-August. Influenza A predominated, accounting for 88% of cases, while influenza B made up 12% of notifications. While the majority of the influenza A cases were unsubtyped (69%), of those subtyped, A(H1N1)pdm09 (33%, 6,922/20,953) was predominant nationally throughout the season, with increasing proportions of A(H3N2) virus towards the end of the season.
Rates of influenza were highest among those in the less than 5 years, 30–44 years and ≥80 years age groups. The age distribution, especially in the younger and middle aged populations, is consistent with the observations of previous years associated with influenza A(H1N1)pdm09 virus, whereas infections in older age groups are typical of influenza A(H3N2).
Taking into account additional data from other targeted influenza surveillance systems monitored throughout the season, the severity of the 2014 influenza season was moderate across most jurisdictions. However, more severe activity was noted in New South Wales, where influenza A(H3N2) circulated at higher levels and affected people in older age groups, which led to a substantial number of outbreaks in residential care facilities.
Invasive Haemophilus influenzae type b
Hib is a gram negative bacterium that causes disease with symptoms dependant on which part of the body is infected. Clinical categories of invasive disease caused by Hib 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); and a range of other infections. Hib is mostly carried as a commensal (present without causing symptoms) in the nasopharynx of healthy individuals and is spread by respiratory secretions, including aerosol transmission or contact with articles soiled with discharges from the nose or throat.77 The case fatality rate of Hib meningitis is at least 3% in developed countries, even with treatment. Approximately 15% to 30% of survivors have permanent neurological sequelae.78
Epidemiological situation in 2014
In 2014, there were 21 notifications of invasive Hib infection in Australia. This was similar to the number of cases notified in 2013 (n=20) and represented a ratio of 1.1 compared with the mean of the previous 5 years. The 2014 notification rate was 0.1 per 100,000 population, consistent with the very low rates seen since the introduction of the vaccine on the NIP in July 1993 (Figure 57). Cases occurred in 6 states or territories, with 9 cases reported in Queensland, 6 cases in New South Wales, 3 cases in Victoria and 1 case each reported in the Northern Territory, South Australia and Western Australia. Notification rates were consistent between states and territories, ranging from 0.1 per 100,000 in New South Wales, South Australia and Victoria to 0.4 per 100,000 in the Northern Territory. There was 1 Hib associated death in 2014 reported in a 2-month-old Indigenous female who was unvaccinated.
Age and sex distribution
Just over half of notified invasive Hib cases in 2014 were male (57%, n=12). Approximately half of the cases (52%, n=11) were in children aged less than 14 years, and 46% (n=5) of these were among infants less than 1 year of age (Figure 58). Consistent with previous years, the 0–4 years age group had the highest notification rate (0.5 per 100,000).
Indigenous status was reported for all Hib cases in 2014. Five cases were reported as Indigenous Australians, representing a notification rate of 0.8 per 100,000. This was higher than the average of the previous 3 years (0.5 per 100,000) but lower than 2010 (1.4 per 100,000).
In 2014, persons less than 22 years of age were eligible for Hib vaccination under the NIP during their infancy. Of the 21 Hib cases reported in 2014, 11 were eligible for vaccination. Six cases were 12 months of age or older, and therefore eligible for the full primary vaccine course and the booster. Of these, 4 were partially vaccinated, 1 was not vaccinated and 1 was of unknown vaccination status. Five cases were less than 12 months of age, of which 3 were reported as partially vaccinated (2 doses) and 2 were not vaccinated.
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. Transmission of the bacterium from person to person is usually via the inhalation of infected respiratory droplets. Many of the signs and symptoms of IPD are non-specific including fever, chills, headache, stiff neck and a general feeling of being ‘out-of-sorts’, severe symptoms can include seizures and occasionally coma.22
Epidemiological situation in 2014
There were 1,564 cases reported in 2014, representing a notification rate of 6.7 per 100,000. This notification rate was unchanged from the rate reported in 2013 and maintains the 20% rate reduction observed following the introduction of the 13-valent pneumococcal conjugate vaccine (13vPCV) to the NIP for infants in July 2011.
In 2014, the Australian Capital Territory, New South Wales, Tasmania, South Australia and Western Australia all reported an increase in the number of cases, with South Australia reporting the greatest increase on the previous year (20%, 111 to 133). The Northern Territory, Queensland and Victoria all reported a reduction in the number of cases, with the Northern Territory reporting the greatest reduction when compared with the previous year (26%, 58 to 43). Changes in notification rates in the jurisdictions reflected the changes in the number of cases, with rates ranging from 3.9 per 100,000 in the Australian Capital Territory to 17.6 per 100,000 in the Northern Territory.
Age and sex distribution
In 2014, males accounted for 53% (n=827) of cases of IPD. The rate of disease in males exceeded that in females in all age groups except for the 5–9 years, 15–19 years and 25–29 years age groups (Figure 59).
In 2014, the notification rate for IPD was highest in older Australians and in young children, with an age distribution similar to that seen in 2013.37 In older Australians, the highest notification rate was in those aged 85 years or older (30.0 per 100,000), while the highest rate in children aged less than 5 years was in those aged 1 year (20.8 per 100,000) (Figure 59).
Many respiratory diseases, including IPD, are known to show a distinct seasonal trend that generally peaks during the winter months. In 2014, the seasonal trend of IPD peaked in July (n=213), 1 month earlier than the preceding 3 years.
In 2014, 89% (n=1,398) of IPD cases were reported with a known Indigenous status. Of those with a known Indigenous status, 14% (n=193) were reported as Indigenous. The notification rate in the Indigenous population (31.4 per 100,000) was approximately 6 times the rate in non-Indigenous people (5.3 per 100,000) (Figure 60).
In Australia, pneumococcal vaccination is recommended as part of routine immunisation for the medically at risk, children under 5 years of age, Aboriginal and Torres Strait Islander peoples aged 50 years or over and other Australians aged 65 years or over. More information on the scheduling of the pneumococcal vaccination can be found in The Australian Immunisation Handbook, 10th edition.32 The history of pneumococcal vaccination recommendations and practice is available through the National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases.79
Although there are over 90 S. pneumoniae serotypes, a relatively limited number cause the majority of IPD. Monitoring the profile of S. pneumoniae serotypes causing invasive pneumococcal disease in the community is critical for evaluating the impact of the NIP funded vaccines as well as for the early detection of emerging serotypes and serotype specific outbreaks. IPD serotypes were reported in 95% (n=1,487) of notified cases in 2014.
In 2014, 68% (1,005) of all notifications with a known serotype were a result of a serotype included in the 23vPPV, and 39% (586) were included in the 13vPCV. Across all ages, the most frequently reported serotypes were 3 (n=150), 19A (n=139), 7F (n=132), 22F (n=120), 19F (n=80) and 6C (n=66) with these 6 serotypes accounting for 46% (687) of all notifications with serotype information. Serotypes 3, 19A, 7F and 19F are included in both the 13vPCV and the 23vPPV. Serotype 22F is only included in the 23vPPV and 6C is not covered by a vaccine. The remaining 56% (n=800) of cases were distributed across 58 other different serotypes.
In Indigenous children aged under 5 years, there were 34 notifications, with serotype 23B (n=6) being the most frequently reported serotype. Serotype 23B is not included in the 13vPCV. In non-Indigenous children aged under 5 years, there were 180 notifications, with serotype 19A (n=30) being the most frequently reported serotype. Serotype 19A is included in the 13vPCV.
In 2014, 37% (n=79) of notifications in children aged under 5 years were a result of a serotype included in the 13vPCV. This was similar to the 38% (n=72) of notifications reported in 2013 and maintains the large reduction in notifications in this age group observed following the introduction of the 13vPCV to the NIP.
In Indigenous adults aged 50 years or over, there were 54 notifications, with serotype 3 (n=6) being the most frequently reported serotype. In non-Indigenous adults aged 65 years or over, there were 502 notifications, with serotype 3 (n=51) and serotype 22F (n=51) being the most frequently reported. Both serotypes 3 and 22F are included in the 23vPPV.
In 2014, 57% (n=31) of notifications in Indigenous peoples aged 50 years or over, and 55% (n=278) of notifications in non-Indigenous Australians aged 65 years or over, were a result of a serotype included in 23vPPV. This continues a general downward trend observed in both these adult population groups in recent years. The 13 serotypes included in the 13vPCV are also included in the 23vPPV and the downward trend in notifications caused by serotypes included in the 23vPPV is likely to be a result of the herd immunity effect afforded to them by the vaccination of infants with 13vPCV.
Enhanced surveillance data sets
Enhanced data are available for IPD notifications. Further analyses, including risk factors and antibiotic susceptibilities can be found in annual and quarterly IPD surveillance report series published regularly in CDI. In addition, a subset of IPD notification data, including serotype, age, sex, Indigenous status, clinical categories and vaccination history are publicly available in the NNDSS IPD Public Dataset (http://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-nndss-ipd-reports.htm).
Measles is a highly infectious acute viral illness, caused by the measles virus, which is spread by respiratory secretions, including aerosol transmission.80 Initial symptoms last 2 to 4 days and are characterised by fever and malaise, followed by a cough, coryza and conjunctivitis. It is usually followed by a red blotchy rash, which typically begins on the face, and then becomes generalised. Measles is often a severe disease with complications more common in the chronically ill, including otitis media, pneumonia, diarrhoea and acute encephalitis.81 Subacute sclerosing panencephalitis is a late, rare (approximately 1 in 100,000 cases) complication of measles caused by persistent infection and is always fatal.32 Complications are more common in children under 5 years of age and in adults over 20 years of age.82
Epidemiological situation in 2014
In 2014, there were 340 notifications of measles. This represents a notification rate of 1.4 per 100,000 population, which was 2.3 times the mean of the previous 5 years (n=146) and an increase of 110% compared with 2013 (n=162) (Figure 61). In 2014, cases of measles occurred in all states and territories, with the 23% of cases occurring in Victoria (n=77) (Figure 62).
In temperate climates and where measles transmission remains endemic, the majority of cases usually occur in late winter to early spring.83 In Australia, this seasonal pattern is no longer evident (Figure 62).
Age and sex distribution
The majority of notified measles cases were male (59%, n=199) in 2014. There was a wide variation in the male to female rate ratio across the age groups with the most notable difference in the 20–24 years and 30–34 years age groups, where there were 2 times as many males as females (Figure 63).
In 2014, age at diagnosis ranged from 0–64 years, with a median age of 19 years. Compared with 2013, notification rates increased in all age groups in 2014. Consistent with recent years, infants less than 1 year of age had the highest age specific rate (10.7 per 100,000). Rates have remained below 2.5 per 100,000 in all age groups between 2009 and 2014, with the exception of the less than 1 year age group in 2011, 2012 and 2014 and the 10–19 years age group in 2014 (Figure 64).
Forty-nine cases occurred in those born between 1978 and 1982 (32–36 years old in 2014), a cohort previously identified as susceptible to measles infection.84 Four cases were born before 1966, a cohort that is considered to have high levels of natural immunity.85
Two doses of the measles containing vaccine are recommended for all persons born during or after 1966. Of the 340 cases notified in 2014, 90% (n=305) were born after 1965 or were 12 months of age or older and therefore eligible for at least 1 dose of a measles-containing vaccine. Eighty-three per cent (n=252) of cases eligible for vaccination were either not vaccinated (42%, 127/305) or of unknown vaccination status (41%, 125/305). Of the remaining 17% (n=53) who were vaccinated, 11 had received the full course of 2 doses of a measles-containing vaccine and 42 were partially vaccinated with 1 dose (Figure 65). Young children and adolescents between 5 and 19 years of age accounted for 61% (77/127) of all unvaccinated cases. In 2014, 28% (25/88) of cases less than 15 years of age were reported as of unknown vaccination, in contrast to 46% (100/217) of cases 15 years or over (Figure 65).
The measles-mumps-rubella (MMR) vaccine induces long term measles immunity in 95% of recipients after a single dose and 99% of recipients after the second dose.32
Indigenous status was completed for 96% of cases in 2014 (n=327), an increase in completeness compared with the 93% of cases in 2013. Of the cases reported in 2014, 3% (n=11) were reported as Indigenous.
Source of infection and outbreaks
Seventy-five per cent of cases in 2014 were either imported (n=140) or import-related (n=115) with the remaining 25% (n=85) of unknown source (Figure 66). Of the imported cases, 64% (90/140) were from the WHO Western Pacific Region, with the majority of cases imported from the Philippines (n=50) followed by Papua New Guinea (n=20) and Vietnam (n=13). Of the remaining imported cases, 43 were imported from the WHO South East Asia Region, 2 from the WHO European Region and 1 from the African Region.
There were 42 clusters of 2 or more epidemiologically linked cases (outbreaks) in 2014 accounting for 60% (n=204) of all cases. The remaining cases comprised sporadic imported cases (n=98) and sporadic cases acquired in Australia of unknown source (n=38). Seventy-eight per cent of clusters were import related (33/42). There were 9 clusters of locally acquired cases of unknown source, which occurred in 6 separate states or territories including Western Australia, 1 cluster of 5 cases; New South Wales, 3 clusters – 1 of 2 cases, 1 of 3 cases and another of 7 cases; Queensland, 1 cluster of 8 cases; the Australian Capital Territory, 1 cluster of 4 cases; The Northern Territory, 1 cluster of 3 cases; Victoria, 1 cluster of 11 cases; and 1 cluster of 6 cases involving both Victoria and the Northern Territory.
Transmission was interrupted quickly in all outbreaks in 2014. The median outbreak duration was 14 days (range 0 to 72 days) between the onset of symptoms in the index and the last case. The median generations of transmission 86 was 1 (range 0 to 7). Thirty-nine of 42 clusters had fewer than 10 cases with a median of 3 cases (range 2 to 9). Of the 3 outbreaks with 10 or more cases, 2 were import related and all were genotyped as B3. The largest of these outbreaks comprised 29 cases and occurred principally in the Northern Territory (n=28), with 1 linked case in a resident of Western Australia. This outbreak commenced in mid-January, lasted approximately 7 weeks, included 5 generations of transmission and was associated with an imported case from Singapore.
Genotyping data were available for 41 clusters with 2 or more linked cases in 2014. Genotype B3 was associated with 22 separate clusters (n=126 cases), D8 with 11 clusters (n=47 cases), D9 with 4 clusters (n=14 cases) and H1 with 4 clusters (n=14 cases). Of the 136 sporadic cases 84% (n=114) were genotyped.
Imported genotypes varied by WHO region. In 2014, there was 1 B3 importation from the African Region and 2 separate D8 importations from the European Region. Multiple genotypes were imported from the South East Asia Region (B3, D8, D9, H1 and G3) and the Western Pacific Region (B3, D8, D9 and H1).
The increasing prevalence of measles in some parts of the world, and the continued circulation of the virus in countries of close geographical proximity to Australia, will result in a continual source of imported virus in Australia. This was particularly the case in 2014 with 157 separate importations occurring. Despite this large number of importations in 2014, the majority were sporadic (n=98) and did not lead to local transmission.
Evidence suggests that endemic measles has been eliminated from Australia, since at least 2005,83 and this was verified by the WHO in 2014.87 In 2014, none of the outbreaks persisted for more than 12 months and there was no evidence of a single genotype continuously circulating. Ongoing evidence of high population immunity was demonstrated by the short duration and small number of cases in the majority of outbreaks.
Due to the highly infectious nature of measles, local transmission and outbreaks will continue to occur in Australia, mostly among susceptible contacts of non-immune travellers from countries where measles remains prevalent.
Mumps is an acute viral illness caused by the mumps virus. Transmission is usually by respiratory secretions, including aerosol transmission, or by direct contact with saliva. Asymptomatic infections occur in one-third of cases. Symptomatic disease ranges from mild upper respiratory tract infections to systemic involvement. The characteristic bilateral, or occasionally unilateral, parotid swelling occurs in 60% to 70% of clinical cases, however, a high proportion have non-specific symptoms including fever, headache, malaise, myalgia and anorexia.88 Mumps encephalitis has been estimated to occur in 1 to 2 per 10,000 cases, with a case fatality rate of around 1%.22
Epidemiological situation in 2014
In 2014, there were 190 notifications of mumps, which was a 13% decrease compared with the 218 cases reported in 2013 and a ratio of 1.1 compared with the 5-year mean (n=167). Since 2009, the national notification rate of mumps has remained below 1.0 per 100,000, ranging from 0.4 per 100,000 in 2010 to 0.9 per 100,000 in 2012 and 2013, and 0.8 per 100,000 in 2014. Cases of mumps were reported from all states and territories in 2014, with the highest rates occurring in South Australia and New South Wales (1.1 per 100,000 each) (Figure 67).
Place of acquisition was complete for 54% (n=102) of cases in 2014, of which 25% (25/102) were imported from overseas: 13 from Asia, 4 from Africa, 4 from the Americas, 2 from Europe and 1 each from the Middle East and New Zealand. The remaining 77 cases were reported as locally acquired in Australia.
Age and sex distribution
In 2014, just over half of all of notified mumps cases were reported in males (52%, n=98) and persons under the age of 40 years (67%, n=128) (Figure 68). The highest number of notifications for males occurred in the 0–4 years age group with 13 cases, while for females notifications were highest in the 35–39 years age group with 11 cases. Consistent with recent years, adults in the 30–39 years age group had the highest rates of infection (1.4 per 100,000) (Figure 69). Since 2010, there has been a steady increase in age-specific rates across all age groups. This is particularly evident in the 1–4 years age group rates, which have increased from 0.3 per 100,000 in 2010 to 1.1 per 100,000 in 2014.
Indigenous status was reported for 77% (n=147) of notified mumps cases in 2014. This is higher than the mean completeness of the previous 5 year period (64%, range 51% to 80%). Of the cases with a known Indigenous status, 3 (2%) were reported as Indigenous. The proportion of mumps notifications reported as Indigenous has remained below 5% since 2010.
The mumps vaccine was first funded on the NIP schedule in 1982 for infants at 12 months of age, with people born after 1980 eligible for at least 1 dose of a mumps containing vaccine. Of the 190 cases notified in 2014, 49% (n=94) were eligible for at least 1 dose of a publicly funded mumps-containing vaccine. Of these, 17% (16/94) were unvaccinated and 38% (36/94) were of unknown vaccination status, 23% (22/94) were fully vaccinated, having received 2 doses of a mumps containing vaccine and 15% (14/94) were partially vaccinated with 1 dose of a mumps containing vaccine. Six cases were reported as vaccinated but had no dose information provided.
The mumps component of the MMR vaccine is considered to be the least effective of the 3 components with the reported 1 dose vaccine effectiveness varying between 60% and 90%.89–91 While protection is greater in 2-dose vaccine recipients, recent outbreaks have been reported in 2-dose recipients, particularly young adults who received their vaccines more than 10 years previously.92,93 Reduced effectiveness of the mumps vaccine over time may partially account for the proportion of vaccinated cases notified and contribute to mumps outbreaks in older vaccinated populations.94
The outbreak reference field was completed for 6% (n=11) of cases in 2014. There were 3 outbreaks of 2 or more epidemiologically linked cases reported, of which, 2 were import related, 1 in Western Australia consisting of 3 cases, and 1 in South Australia consisting of 5 cases. The third outbreak comprised of 2 locally acquired cases in Western Australia.
Pertussis, commonly known as whooping cough, is a highly infectious acute respiratory disease caused by the bacteria Bordetella pertussis. Spread by respiratory droplets, infection is often characterised by paroxysmal cough with inspiratory whoop, which is frequently seen among unvaccinated children but uncommon in individuals who have acquired some immunity through vaccination or infection.95 The highest risk of infection and severe morbidity from pertussis occurs in infants who are too young to have received at least 2 doses of a pertussis-containing vaccine.32 Complications include pneumonia, atelectasis, seizures, encephalopathy, and hernias, with pneumonia as the most common cause of death.22
Epidemiological situation in 2014
In 2014, pertussis notifications were at their lowest levels since 2007 and continued to display a downwards trend since reaching a peak in 2011, at the height of the most recent epidemic period, 2008 to 2012. There were 11,863 notifications of pertussis, which was a 4% decrease in notified cases compared with 2013 (n=12,362) and 51% less than in 2012 (n=24,101) (Figure 70). There were 2 pertussis related deaths reported. Both of these cases were reported as unvaccinated, with 1 case aged 7 months and the other 85 years.
In 2014, all jurisdictional specific rates had returned to pre-epidemic levels with rates remaining below 90 per 100,000 population. Compared with 2013, rates declined in all jurisdictions except New South Wales, Victoria and Western Australia (Figure 71). Rates in Victoria increased from 51 per 100,000 in 2013 to 81 per 100,000 in 2014, in New South Wales from 32 per 100,000 in 2013 to 42 per 100,000 in 2014 and in Western Australia from 65 per 100,000 in 2013 to 68 per 100,000 in 2014.
Age and sex distribution
Males accounted for 56% (n=6,657) of cases in 2014 and had higher rates across all age groups from 10 years of age (Figure 72). The highest notification rate in both males and females occurred in the 10–14 years age group at 126 and 117 per 100,000 respectively.
In 2014, children less than 15 years of age represented 37% (n=4,407) of notifications and had a notification rate (100 per 100,000) 2.6 times higher compared with those 15 years of age or over (36 per 100,000). After reaching a peak in 2011 rates in children less than 15 years of age have declined steeply, with the ratio of cases under 15 years compared with those over 15 years falling from 3.7 in 2011 to 2.7 in 2014. The highest age specific rates in 2014 occurred in the 10–14 years age group (122 per 100,000), which was higher than the rates reported in 2013 (111 per 100,000) (Figure 73).
The NIP schedule in 2014 included a primary course of 3 doses of vaccine at 2, 4, and 6 months of age, with additional booster doses provided at 4 years of age and between 10 and 15 years of age.32
In order to determine the vaccination status of cases, public health follow-up is required. As per the pertussis national guidelines for public health units,96 jurisdictions prioritise case follow-up to those less than 5 years of age. During 2014, those aged less than 5 years accounted for 9% (n=1,117) of all notified cases, of which information about vaccination status was available for 89% (n=992).
Of the children eligible to receive a pertussis-containing vaccine in 2014, 33% (n=255) of cases had received the full primary course of 3 doses and 22% (n=34) had received the full scheduled course of 4 doses (Table 18). Fifty-nine per cent (n=636) of eligible cases less than 5 years of age had received at least 2 doses of a pertussis-containing vaccine in 2014.
|Age group||Number of vaccine doses||Unknown||Total|
|Less than 6 weeks of age
(not eligible for vaccination)
|6 weeks to <4 months
(eligible for 1 dose of vaccine)
|4 to < 6 months
(eligible for 2 doses of vaccine)
|6 months to < 4 years
(eligible for 3 doses of vaccine)
|4 to 5 years
(eligible for 4 doses of vaccine)
Pertussis vaccine effectiveness among 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 2003.97 Immunity to disease decreases over time post-vaccination, with estimates of protection remaining for 4 to 12 years.98–100 While pertussis can affect people of any age, infants are at highest risk of more severe disease as adequate immunity is not achieved through infant vaccination until receiving at least the second vaccine dose at 4 months of age.101
Epidemics of pertussis have historically occurred at regular intervals of approximately 4 years on a background of endemic circulation in Australia, with the most recent epidemic peaking in 2011. In 2014, all jurisdictions reported pertussis activity consistent with pre-epidemic levels and national rates were at their lowest since 2007. However nationally, an increasing trend was evident from mid-2014, which was driven by a significant increase in pertussis activity in New South Wales and Victoria and a return to epidemic level activity in 2015 would not be unexpected.
All jurisdictions, except for the Northern Territory, ceased their respective cocooning programs in 2012, which included various combinations of providing free booster vaccinations to mothers and carers of infants.
Poliomyelitis is an acute illness following gastrointestinal infection by 1 of the 3 types of poliovirus. Transmission occurs primarily from person-to-person via the faecal-oral route. In most cases poliovirus infection is not symptomatic but, in less than 1% of cases the virus may invade the nervous system and cause acute flaccid paralysis (AFP).22
Epidemiological situation in 2014
In 2014, there were no notifications of poliomyelitis. Australia, along with the Western Pacific Region, remains poliomyelitis free.
Poliovirus infection, both paralytic (poliomyelitis) and non-paralytic, is a notifiable disease in Australia. Clinical and laboratory investigation is conducted for cases involving patients of any age with a clinical suspicion of poliomyelitis, following the WHO protocol, which focuses on investigating cases of AFP in children under 15 years of age. The WHO target for AFP surveillance in a polio free country is 1 case of AFP per 100,000 children less than 15 years of age. Australia has achieved this surveillance target since 2008. However, the virological surveillance indicator of adequate stool specimen collection in 80% of AFP cases has never been met. More details can be found in the annual report series published in the CDI by the Australian Enterovirus Reference Laboratory who coordinate poliovirus surveillance activities in Australia.
Rubella and congenital rubella
Rubella is a rare disease in Australia.
Rubella is generally a mild and self-limiting infectious disease caused by a rubella virus. It is spread from person-to-person through contact with respiratory secretions, including aerosol transmission. A rash, usually starting on the face before spreading across the body, may appear around 2 weeks after exposure to the virus and usually lasts for 3 days. Children usually show few or no constitutional symptoms of infection, but adults may experience 1 to 5 days of early low grade symptoms, such as fever, malaise, headaches and mild head colds.22 Clinically, rubella can be difficult to distinguish from other diseases that also cause febrile rash, such as measles, and is asymptomatic in up to 50% of cases.
Rubella infection in the first trimester of pregnancy can result in miscarriages, foetal deaths or stillbirths, and a collection of birth defects known as congenital rubella syndrome (CRS) in over 90% of cases.22,102 CRS can result in single or combined defects such as hearing impairment, eye abnormalities (including retinopathy, cataract and microphthalmia) congenital glaucoma, microcephaly, meningoencephalitis, development delay, purpura, jaundice radiolucent bone disease and congenital heart disease.
Epidemiological situation in 2014
In 2014, there were 17 cases of rubella reported, representing a rate of 0.1 per 100,000. While this was consistent with the low rates of this disease experienced since 2003, it was a marked decline from the peak rate of more than 7.5 per 100,000 in 1997 (Figure 74). Cases were reported from all states except Tasmania. No cases were reported from the Australian Capital Territory or the Northern Territory. There were no cases of CRS reported in 2014.
Age and sex distribution
In 2014, the majority of notified rubella cases were female (65%, n=11), of which 64% (7) were of child bearing age (15–44 years of age) (Figure 75). The median age of cases was 35 years, with a range of 7–56 years. Consistent with previous years, the majority of cases (82%, 14/17) occurred among adults over the age of 20 years (Figure 75), and age-specific rates remained below 0.7 per 100,000 across all age groups (Figure 76).
Rubella vaccine is provided in the combined MMR or measles-mumps-rubella-varicella vaccine, and in 2014 was provided under the NIP schedule at 12 months and 18 months of age. A dose at 4 years of age was also recommended for those who did not receive the second dose at 18 months of age.32
Of the 17 cases notified in 2014, 4 were reported as vaccinated; 1 fully vaccinated, receiving 2 doses of a rubella-containing vaccine; 1 as partially vaccinated, receiving 1 dose; and 2 reported as vaccinated with no dose information provided. Two were reported as not vaccinated and the remaining 11 were of unknown vaccinations status.
The primary aim of immunisation against rubella is to prevent cases of CRS.103 Two doses of a rubella-containing vaccine are recommended for all non-immune persons born during or since 1966 and who are greater than 18 months of age.
Evidence suggests that endemic rubella is well controlled in Australia. A marked decline in rubella notifications since 2003 has seen rates in Australia remain well below the 1.0 per 100,000 population WHO goal indicative of rubella control.104 The increasing trend in age of notifications likely reflects the declining rates of rubella among children since routine MMR immunisation was implemented and the subsequent achievement of high 2 dose coverage. Males, historically more susceptible as universal vaccination was not introduced until 1989, no longer appear to be at greater risk of infection compared with females.
CRS is rare in Australia and in recent years has mainly occurred among infants of women who were born overseas.105
Tetanus is an acute, often fatal, disease caused by the toxin produced by the bacterium Clostridium tetani. C. tetani spores usually enter the body through contamination of a wound with manured soil. 22 The neurotoxin acts on the central nervous system to cause muscle rigidity with painful spasms. Generalised tetanus, the most common form of the disease, is characterised by increased muscle tone and generalised spasms. The disease usually occurs after an incubation period of 3 to 21 days (ranging from 1 day to several months), with a median time of onset at 10 days post injury. In Australia, tetanus is rare occurring primarily in older adults who have never been vaccinated or have not received a booster dose in the past 10 years. A high level of diagnostic awareness of tetanus is important in the elderly, as most deaths occur in people over 70 years of age, especially females, and may be associated with an apparent minor injury.106
Epidemiological situation in 2014
In 2014, there were 3 notifications of tetanus (Figure 77). This was consistent with the low number of this disease notified in recent years. All cases were adult males 30 years of age or over. Place of acquisition was reported for all cases, with 1 case reported to have acquired their infection in Italy and 2 in Australia. There were no reported deaths due to tetanus in 2014.
The NIP schedule in 2014 recommends a primary course of tetanus vaccination including 3 doses provided at 2, 4, and 6 months of age. Two booster doses are provided at 4 years and between 10 and 15 years delivered through school based programs. Booster doses are additionally recommended for all adults at the age of 50 years who have not received 1 in the previous 10 years.32
Of the 3 cases notified in 2014, 2 were reported as not vaccinated and 1 was of unknown vaccination status.
Complete immunisation induces protection that lasts throughout childhood but by middle age, 50% of vaccine recipients have low or undetectable levels of antibodies. Tetanus is however uncommon in people who have received 4 or more doses of a tetanus-containing vaccine, and in those who received their last dose within 10 years.105
Varicella zoster virus
The VZV is a highly contagious member of the herpesvirus family and causes 2 distinct illnesses; chickenpox as the primary infection, and shingles (herpes zoster), which occurs following reactivation, often many years later, of latent virus in approximately 20% to 30% of all chickenpox cases. Shingles occurs more frequently among older adults (most commonly after 50 years of age) and in immunocompromised people.22
In 2006, the CDNA agreed 3 categories of VZV infection were nationally notifiable: chickenpox, shingles and varicella zoster virus unspecified. By 2009, all jurisdictions were notifying VZV infections to the NNDSS against these 3 categories, except New South Wales, where VZV is not a notifiable disease.
The ability to categorise a VZV infection as chickenpox or shingles depends on follow-up to determine the clinical presentation of the case. The majority of VZV infections are reported as unspecified as follow-up does not occur (Table 5). Notification rates for chickenpox, shingles and VZV unspecified, including any comparisons made between jurisdictions and age groups, should be interpreted with caution as they are affected by the varying levels of follow-up undertaken in each jurisdiction.
Epidemiological situation in 2014
In 2014, there were 19,658 VZV notifications from the 7 reporting jurisdictions. This was 16% more than the total cases notified in 2013 (n=16,986). Of the total VZV notifications in 2014, 62% (n=12,097) were reported as unspecified VZV infection, 28% (n=5,471) as shingles and 12% (n=2,088) as chickenpox (Figure 78).