Results - continued

Vectorborne diseases

Vectorborne diseases are infections transmitted by arthropods such as such as mosquitoes and ticks. A vectorborne disease may involve a simple transfer via the arthropod, or may involve replication of the disease-causing agent in the vector.¹⁹ Vectorborne diseases of public health importance in Australia listed in this chapter are: arbovirus NEC; Barmah Forest virus (BFV) infection; dengue virus (DENV) infection; Japanese encephalitis virus (JEV) infection; Kunjin virus (KUNV) infection; malaria; Murray Valley encephalitis virus (MVEV) infection; and Ross River virus (RRV) infection. The vectorborne diseases yellow fever virus infection, plague and certain viral haemorrhagic fevers are listed under quarantinable diseases. The National Arbovirus and Malaria Advisory Committee (NAMAC) provide expert technical advice on vectorborne diseases to the Australian Health Protection Principal Committee through the CDNA. NAMAC provides a detailed report of vectorborne diseases of public health importance in Australia by financial year.⁹⁷

Alphaviruses

Viruses in the genus Alphavirus that are notifiable in Australia are BFV and RRV. These viruses are unique to the Australasian region.⁹⁸ Infection can cause a clinical illness, which is characterised by fever, rash and polyarthritis. The viruses are transmitted by numerous species of mosquito that breed in diverse environments.⁹⁹ The alphavirus chikungunya is not presently nationally notifiable, and thus not included in this annual report. However, it is notifiable in all states and territories except the Australian Capital Territory, and states and territories send information about cases to the Commonwealth for national collation and analysis.^97,100

The national case definitions for RRV and BFV require only a single IgM positive test to one virus, in the absence of IgM to the other.¹⁰¹ False positive IgM diagnoses for BFV in particular are a known issue, thus it is unclear what proportion of notifications represent true cases. There was a large increase in notifications of BFV nationally from October 2012, which was likely to have been due to false positive notifications.

Barmah Forest virus infection

Epidemiological situation in 2012

In 2012, there were 1,722 notifications of BFV infection, equating to a rate of 7.6 per 100,000 population. This compares with a 5-year mean of 1,718 notifications and a 5-year mean rate of 7.9 per 100,000. The number of notifications of Barmah Forest virus increased sharply from October 2012 (Figure 68). This increase continued into late 2013 and beyond for some jurisdictions. The increase was considered likely to have been due to a high rate of false positive IgM test results from the use of a commercial test kit in private laboratories, and resulted in a recall of the affected kits in September 2013.¹⁰²

Figure 68: Notifications of Barmah Forest virus infection, Australia, 2007 to 2012, by month and year and state or territory

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Seasonality and place of acquisition

The seasonality of BFV notifications is less marked than for RRV, and a high proportion of interseasonal notifications are thought to be due to false positive diagnoses. The peak notifications of BFV between 2007 and 2012 was between January and April, and 45% of cases were diagnosed during these months (compared with 55% for RRV). The increase from October 2012 was earlier than the expected seasonal increase.

More than half of all BFV notifications in 2012 were from Queensland (57%) and rates were highest in the Northern Territory (37.0 per 100,000) and Queensland (21.5 per 100,000).

Age and sex distribution

BFV was most frequently reported in middle aged adults (median 46 years, range 0–86 years). Age and sex specific rates were highest among males aged 45–49 years females aged 60–64 years (Figure 69).

Figure 69: Notification rates for Barmah Forest virus infection, Australia, 2012, by age group and sex

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Ross River virus infection

Epidemiological situation in 2012

In 2012, there were 4,683 notifications of RRV; a rate of 20.6 per 100,000. This compares with a 5-year mean of 4,953 notifications and a 5-year mean rate of 22.8 per 100,000.

Seasonality

The peak in notifications for RRV from 2007 to 2012 occurred between January and April, and 55% of cases were diagnosed during these months (Figure 70).

Figure 70: Notifications of Ross River virus infection, Australia, 2006 to 2012, by month and year and state or territory

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Between 2007 and 2012, nearly half of all RRV infections were from Queensland (42% of all cases, 42.6 cases per 100,000), but population rates were highest in the Northern Territory (96.5 per 100,000).

Age and sex distribution

RRV was most frequently reported in adults aged in their 30s or 40s (median 42 years, range 0–85 years). Age specific rates were highest among females in the 40–44 years age group and for males in the 35–39 years age group (Figure 71).

Figure 71: Notification rates for Ross River virus infection, Australia, 2012, by age group and sex

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Flaviviruses

In Australia, flavivirus infections of particular public health importance are DENV, KUNV, MVEV and JEV. Unspecified flavivirus infections are reported under arbovirus NEC. These infections are nationally notifiable.

DENV has 4 serotypes, each containing numerous genotypes. The serotypes isolated from returning travellers (and thus involved in local outbreaks) vary by year and geographical region. Infection with 1 serotype probably confers lifelong immunity to that serotype,¹⁹ but subsequent infection with a different serotype is one factor thought to increase the risk of severe outcomes, along with the infecting serotype and genotype and host factors.^19,103–105 The clinical illness is characterised by mild to severe febrile illness with fever, headache, muscle or joint pain and sometimes a rash. A minority of cases progress to severe dengue with haemorrhage and shock. Aedes aegypti is the major vector of DENV in Australia.

Infection with MVEV, KUNV or JEV is usually asymptomatic or produces a non-specific illness, but a small percentage of cases progress to encephalomyelitis of variable severity. Culex annulirostris is the major vector of MVEV, JEV and KUNV. No specific treatment is available for these diseases and care is largely supportive. A vaccine is available to prevent JEV infection,²⁰ but there are no vaccines currently for DENV, MVEV or KUNV infection.

Arbovirus NEC

Epidemiological situation in 2012

In 2012, there were 9 notifications of arbovirus NEC, compared with an average of 16.2 during the previous 5 years. These notifications comprised Alfuy (1 case), flavivirus unspecified (4 cases), Zika (1 case), Kokobera (2 cases) and Stratford (1 case), (Table 20).

Table 20: Notifications of arbovirus NEC, Australia, 2012, by infecting agent and state or territory

State	Organism	Country of acquisition	Age
Qld	Alfuy	Unknown	55
Qld	Kokobera	Unknown	51
Qld	Kokobera	Unknown	68
Qld	Untyped	Australia	20
Qld	Untyped	Cambodia	43
Qld	Untyped	Thailand	22
Qld	Untyped	Philippines	56
Qld	Stratford	Unknown	70
SA	Zika	Indonesia	53

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Information on the place of acquisition was available for 44% of cases (4/9), and three of these were acquired overseas.

The median age of cases was 53 years (range 20–70 years).

Dengue virus infection

Local transmission of dengue in Australia is normally restricted to areas of northern Queensland where the key mosquito vector, Ae. aegypti is present.¹⁰⁶ Dengue is not endemic in North Queensland, but local transmission can occur upon introduction of the virus to the mosquito vector by a viraemic tourist or a resident returning from a dengue-affected area overseas.¹⁰⁷

The CDNA case definition for dengue was changed in 2013 to accept dengue non-structural protein 1 (NS1) antigen in blood as laboratory definitive evidence for infection; however, it should be noted that a number of states and territories had been sending notifications based on a positive NS1 antigen prior to this change.

Epidemiological situation in 2012

There were 1,540 notifications of dengue in 2012, with 817 in 2011. This was 1.8 times the 5-year mean of 864 notifications. Most infections were acquired overseas (n=1,410) (Figure 72). There were 29 infections acquired in Australia. For 101 cases, no information was supplied on the place of acquisition.

Figure 72: Notifications of dengue virus infection, Australia, 2007 to 2012, by month, year and place of acquisition

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Serotype of dengue virus infections

In 2012, serotype information was available for 18% of notifications (282/1,540), which was a decrease compared with the 5-year mean of 50% (Table 21). The decreased reporting of a serotype may reflect the increasing use of NS1 antigen detection and/or other diagnostic methods that do not provide a serotype. In 2012, 49% (137/282) of cases with a known serotype were due to DENV serotype 2 and 28% (79/282) were DENV 1 (Table 21).

Table 21: Serotype of dengue virus infections, Australia, 2007 to 2012

Serogroup	2007	2008	2009	2010	2011	2012
Virus 1	36	40	82	190	139	79
Virus 1 and 4	1					1
Virus 2	14	32	54	255	153	137
Virus 2 and 3	1
Virus 3	52	143	771	106	78	57
Virus 4	7	37	43	47	43	8
Untyped/unknown	203	309	452	629	404	1,258
Total	314	561	1,402	1,227	817	1,540
% with a serotype supplied	35.4	44.9	67.8	48.7	50.6	18.3

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Seasonality and place of acquisition

There were 1,412 DENV infections known to have been acquired overseas in 2012, up from 714 in 2011 and the largest number ever reported. Between 2007 and 2010, the number of DENV cases known to have been acquired overseas increased each year, from 254 in 2007 to 1,137 in 2010 (Figure 72). In recent years, improved diagnostic techniques, in particular the availability of the rapid NS1 antigen detection kit, have improved detection and would have contributed to the observed increase in reported numbers of overseas-acquired dengue in Australia,¹⁰⁸ along with the dramatic re-emergence and geographical expansion of dengue overseas over the past 50 years and explosive outbreaks.¹⁰⁵

For 99 cases (6%), no information on the place of acquisition was available, and no particular country or region of acquisition was stated for 5 cases that were known to have been acquired overseas, (Table 22). Cases acquired in Indonesia continue to account for the largest number and proportion of all notifications, accounting for 54% (778/1,441) of all cases in 2012, but down from the 58% in 2010 and compared with an average of 33% over the previous 5 years. DENV acquired in Indonesia was frequently serotype 2, comprising 76% of cases with a known serotype (101/132 cases). Other frequently reported source countries in 2012 included Thailand, India, the Philippines and East Timor.

Table 22: Serotype of dengue virus notifications, Australia, 2012, by serotype and place of acquisition

Place of acquisition	Serotype					Untyped/ unknown	Total
	DENV 1	DENV 1 and 4	DENV 2	DENV 3	DENV 4
Locally acquired
Australia	14	0	2	7	0	6	29
Unknown
Unknown/not stated	1	0	1	0	0	97	99
Overseas acquired
Indonesia	20	0	101	8	3	646	778
Thailand	21	0	17	11	2	204	255
India	3	0	2	9	0	44	58
Philippines	3	1	2	1	1	45	53
East Timor	1	0	1	12	0	36	50
Fiji	6	0	2	0	0	22	30
Cambodia	1	0	0	0	0	28	29
Sri Lanka	2	0	1	2	0	20	25
Vietnam	1	0	2	1	0	16	20
Malaysia		0	2	0	1	15	18
Papua New Guinea	1	0	1	4	0	10	16
Bangladesh		0	0	0	0	12	12
Kiribati	2	0	0	0	0	5	7
Maldives	1	0	0	0	0	3	4
Burma (Myanmar)	1	0	0	0	0	2	3
Other countries	1	0	2	2	1	43	49
Country not stated	0	0	1	0	0	4	5
Total overseas acquired	64	1	134	50	8	1,155	1,412
Total	79	1	137	57	8	1,258	1,540

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All but one of the 29 locally-acquired DENV in 2012 were known to have been associated with one of the 5 outbreaks of locally-acquired infection in Queensland in 2012 that were notified to NNDSS. The largest number of notified cases during the year was during an outbreak of DENV 1 and 2 in Townsville with 8 cases notified to NNDSS in 2012. An outbreak in Cairns, which began in late 2012 was larger, with a total of 146 cases, but most of these (141) were notified in 2013.

The peak months for overseas-acquired dengue in 2012 were January to April, together accounting for 58% (821/1,412) of cases. No particular pattern was evident with the small number of locally-acquired cases; however, there was only 1 case between July and October 2012, demonstrating that outbreaks are not continuing through the cooler months.

Age and sex distribution

DENV infections acquired overseas in 2012 were most commonly reported among younger and middle aged adults (median 39 years, range 2–85 years), with a peak of notifications among males aged 20–29 years and females aged 25–29 years (Figure 73). Males comprised 51% of cases with overseas-acquired DENV. For locally-acquired DENV, infections were more commonly reported among middle aged and older adults (median 44 years, range 5–76 years), with peak notifications among males and females aged 40–44 years (Figure 74). Males comprised 45% of cases with locally-acquired DENV.

Figure 73: Notifications of overseas-acquired dengue, Australia, 2012,* by age group and sex

* Sex was not available for 2 cases.

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Figure 74: Notifications of locally-acquired dengue virus infection, Australia, 2012, by age group and sex

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Kunjin virus infection

Epidemiological situation in 2012

In 2012, there were no notified KUNV infections in Australia, compared with 2 cases in 2011 and an average of 1.6 cases per year between 2007 and 2011.

Japanese encephalitis virus infection

Epidemiological situation in 2012

There was 1 notification of JEV infection in 2012, in a 16-year-old female who acquired the infection in the Philippines. Prior to this case there was 1 notification of JEV infection in 2008, which was also acquired overseas. The last locally-acquired case was in 1998.¹⁰⁹

Murray Valley encephalitis virus infection

Epidemiological situation in 2012

In 2012, there was 1 notification of MVEV infection, in a 14-year-old who acquired the infection in Papua New Guinea and was diagnosed in Queensland. In the past 5 years there were 2 cases in 2008, 4 cases in 2009 and 17 cases in 2011. The cases notified in 2011, including an outbreak in south east Australia, have been described elsewhere.^97,110–112

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Malaria

Malaria is caused by a protozoan parasite in the genus Plasmodium, and 5 species are known to infect humans; Plasmodium vivax, Plasmodium falciparum, Plasmodium malariae, Plasmodium ovale and Plasmodium knowlesi.^19,113 Malaria is a serious acute febrile illness that is transmitted from person to person via the bite of an infected mosquito of the genus Anopheles. Australia was declared free of malaria in 1981,¹¹⁴ but suitable vectors are present in northern Australia, and the area remains malaria-receptive. Malaria is the most frequently reported cause of fever in returned travellers worldwide.¹¹⁵ A recent case series in the Northern Territory showed that malaria cases were reported in travellers returning from endemic areas, but also reflected current events such as military operations and increased refugee arrivals from particular areas.¹¹⁶ Malaria cases in Australia can be found either through testing of symptomatic persons with a compatible travel history, or through screening of refugees who may be asymptomatic.

Epidemiological situation in 2012

There were 348 cases of malaria notified in Australia in 2012; a 28% decrease compared with the 5-year mean of 484 notifications, and continuing the trend of gradually decreasing notifications since 2005 (Figure 75). The largest number of cases was reported by Queensland (100 cases).

Figure 75: Notifications of malaria, Australia, 2007 to 2012, by month, year and place of acquisition

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Seasonality and place of acquisition

The place of acquisition was listed as overseas for 297 cases, while for the remaining 51 cases, no place of acquisition information was supplied to NNDSS, but none were known to have been acquired in Australia. The last known locally-acquired infections were in 2011 in an outbreak in the Torres Strait,¹¹⁷ and the last cases acquired on the mainland were during an outbreak in North Queensland in 2002.¹¹⁸

Complete information on the country or region of acquisition was supplied for all but six of the cases known to have been acquired overseas, and these remaining cases were notified as being overseas acquired, country unknown or not stated. The most frequent countries of acquisition were Papua New Guinea (16% of cases with complete information) and India (16%) (Table 23). Most cases acquired in Papua New Guinea were reported by Queensland (31 cases). Increases in notifications or an observable pattern of seasonality in a predominantly overseas-acquired infection can relate to the seasonality of travel patterns or to local disease epidemiology in the source countries. There was no discernible pattern of seasonality in notifications between 2007 and 2011, or in 2012.

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Infecting species

The infecting species was supplied for 99% (343/348) of notifications in 2012 (Table 23). The most frequent infecting species was P. falciparum (reported in 54% of notifications with complete information). P. vivax was associated with Asia and the Pacific, whilst most infections acquired in African countries were P. falciparum. In infections acquired in Papua New Guinea however, P. falciparum and P. vivax infections were reported in similar numbers (20 and 25 cases respectively).

Table 23: Notifications of malaria, Australia, 2012, by infecting species and region and country of acquisition

Country and region	P. falciparum	P. vivax	P. ovale	P. malariae	Mixed species infection	Plasmodiumspecies	Total
nfd - Not further defined.
Oceania
Papua New Guinea	20	25	0	0	0	1	46
Solomon Islands	0	7	0	0	0	0	7
South East Asia
Indonesia	8	8	0	0	0	1	17
Cambodia	2	4	1	0	0	0	7
Philippines	1	2	0	0	0	0	3
Laos	2		0	0	0	0	2
Thailand	0	1	0	0	0	0	1
Malaysia	0	1	0	0	0	0	1
Mainland southeast Asia, nfd*	0	1	0	0	0	0	1
North-east Asia
China	0	1	0	0	0	0	1
Southern and Central Asia
India	4	39	1	0	0	2	46
Pakistan	0	17	0	0	0	0	17
Bangladesh	0	1	0	0	0	0	1
Americas
Guyana	2	1	0	0	0	0	3
Brazil	0	2	0	0	0	0	2
South America, nfd	0	1	0	0	0	0	1
South America, not elsewhere classified	0	1	0	0	0	0	1
North Africa and the Middle East
Sudan	33	1	0	0	0	0	34
North Africa, nfd	2	1	0	0	0	0	3
Iran	1	0	0	0	0	0	1
Sub-Saharan Africa
Ghana	14	0	0	0	0	0	14
Sierra Leone	9	1	1	1	0	0	12
Tanzania	9	0	0	1	0	0	10
Uganda	7	0	1	1	0	1	10
Kenya	6	0	0	2	0	0	8
Nigeria	7	0	0	0	0	0	7
Guinea	6	0	0	0	0	0	6
Other sub-Saharan Africa countries	19	1	2	0	2	0	24
Sub-Saharan Africa countries, nfd	5	0	0	0	0	0	5
Overseas acquired – country and region not stated/unknown
Unknown country	5	0	1	0	0	0	6
Overseas-acquired total	162	116	7	5	2	5	297
Place of acquisition unknown	23	23	3	2	0	0	51
Total	185	139	10	7	2	5	348

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Age and sex distribution

In 2012, sex was stated for all but 1 case. Malaria was most commonly reported in males (70%, 244/347 cases) with a peak of notifications in males aged 20–24 years and 25–29 years (Figure 76). The median age of cases was 31 years (range 1–77 years).

Figure 76: Notifications of malaria, Australia, 2012, by age group and sex*

* Sex was not stated for 1 case, and this case has been excluded.

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Zoonotic diseases

Zoonoses are those diseases and infections that are naturally transmitted between vertebrate animals and humans.¹¹⁹ Approximately 60%–70% of emerging human infectious diseases are zoonoses^120–122 and more than 70% of emerging zoonoses originate from wildlife.¹²¹ An emerging zoonosis is defined by WHO as ‘a zoonosis that is newly recognised or newly evolved, or that has occurred previously but shows an increase in incidence or expansion in geographical, host or vector range’.¹²³

The zoonoses notifiable to the NNDSS included in this chapter are: anthrax, Australian bat lyssavirus or lyssavirus (unspecified) infection, brucellosis, leptospirosis, ornithosis, Q fever, and tularaemia.

Several zoonoses notifiable to the NNDSS are included under other headings in this report. For example, Salmonella and Campylobacter infections are typically acquired from contaminated food and are listed under the gastrointestinal diseases section. Rabies is listed under Quarantinable diseases.

Anthrax

Anthrax is caused by the bacterium Bacillus anthracis and mainly causes cutaneous infection. However, it can also cause gastrointestinal and respiratory infections. Anthrax is primarily a disease of herbivores; humans and carnivores are incidental hosts. It can be an occupational hazard for veterinarians, and agriculture, wildlife and livestock workers who handle infected animals or by-products.

In Australia, the areas of anthrax risk are well defined and include the northern and north-eastern districts of Victoria and central New South Wales.¹²⁴ Anthrax occurs only sporadically in livestock in the at-risk areas. Rare or isolated incidents or cases have historically occurred in Queensland, South Australia, Tasmania and Western Australia.¹²⁴

Epidemiological situation in 2012

In 2012, there were no notified cases of anthrax in Australia. Over the previous 10 years, only 3 human cases of anthrax were reported in Australia; in 2006, 2007 and 2010.^125–127 All had domestic farm or animal related exposures and all were cutaneous anthrax. Australia has never recorded a human case of inhalational or gastrointestinal anthrax.

There were 4 anthrax incidents reported in livestock in Australia in 2012, with all properties located within the known New South Wales anthrax endemic area.¹²⁴

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Australian bat lyssavirus and lyssavirus (unspecified) infections

ABLV belongs to the genus lyssavirus, which also includes the rabies virus. Both invariably result in progressive, fatal encephalomyelitis in humans.¹²⁸ ABLV was identified in Australia in 1996 ^129,130 and is present in some Australian bats and flying foxes. Australia is free of terrestrial rabies.

The best way to prevent ABLV infection is to avoid contact with bats. For people whose occupation (including volunteer work) or recreational activities place them at increased risk of being exposed to ABLV, rabies virus vaccine is effective in preventing infection. Pre-exposure vaccination with rabies virus vaccine is recommended for bat handlers, veterinarians and laboratory personnel working with live lyssaviruses.¹³¹ Post-exposure prophylaxis for ABLV consists of wound care and administration of a combination of rabies virus vaccine and human rabies virus immunoglobulin, depending on exposure category and prior vaccination or antibody status.^20,131

Epidemiological situation in 2012

In 2012, there were no notified cases of ABLV or lyssavirus (unspecified) infection in Australia. There were also no cases of rabies in 2012. Rabies is reported in more detail in the quarantinable diseases section.

There have been 3 fatal cases of ABLV infection in humans, in 1996, 1998 and 2013. All cases occurred after close contact with an infected bat and all were fatal.^132–134 In 2013, the Queensland Department of Agriculture, Fisheries and Forestry confirmed ABLV infection in 2 horses on a Queensland property. These were the first known equine cases of ABLV infection.^135,136

The bat health focus group in the Australian Wildlife Health Network gathers and collates information from a range of organisations on opportunistic testing of bats for ABLV. In 2012, there were 5 ABLV detections compared with 6 detections in bats during 2011.¹³⁷

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Brucellosis

Brucella species that can cause illness in humans include Brucella melitensis acquired from sheep and goats, B. suis from pigs and B. abortus from cattle. B. abortus was eradicated from Australian cattle herds in 1989 and B. melitensis has never been reported in Australian sheep or goats.¹²⁴ Therefore, all cases of B. melitensis or B. abortus in Australia are related to overseas travel. B. suis is confined to some areas of Queensland, where it occurs in feral pigs. Eales et al. (2010)¹³⁸ found that feral pig hunting was the most common risk factor for infection for brucellosis cases in Townsville during 1996 to 2009.

Internationally, brucellosis is mainly an occupational disease of farm workers, veterinarians, and abattoir workers who work with infected animals or their tissues.¹⁹

Epidemiological situation in 2012

In 2012 there were 29 notified cases of brucellosis in Australia (a rate of 0.1 per 100,000), compared with the 5-year mean of 35 notifications (2007 to 2011). Seventy-six per cent of notifications (22/29) were from Queensland (Figure 77), with a rate of 0.5 per 100,000. Since 1991, 84% of notifications have been from Queensland.

Figure 77: Notifications of brucellosis, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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The species of the infecting organism was available for 40% of notifications (12/29). Of these, 9 notifications were for B. suis; eight from Queensland and one from South Australia (abattoir worker), and all were males aged between 20 and 36 years. There were 2 notifications of B. melitensis, with the country of acquisition listed as Iraq and Lebanon. There was also 1 notification for B. abortus from New South Wales, which was listed as having been acquired overseas, but the specific county was unknown.

The median age of notified cases of brucellosis was 36 years (range 18–72 years) and 90% of cases (26/29) were male.

Leptospirosis

Leptospirosis is caused by spirochaetes of the genus Leptospira, which is found in the genital tract and renal tubules of domestic and wild animals. In affected areas, where there is exposure to infected urine of domestic and wild animals, this disease can be an occupational and recreational hazard (such as in certain agricultural sectors and swimming or wading in contaminated water).^139,140 The last reported death in Australia attributed to leptospirosis was in 2002.¹⁴¹

Epidemiological situation in 2012

In 2012 there were 116 notified cases of leptospirosis in Australia (a rate of 0.5 per 100,000), compared with the 5-year mean of 141 notifications (2007 to 2011). Notifications in 2012 returned to expected levels after an increase in 2011 (Figure 78), which was largely attributed to extensive flooding in central and southern Queensland.^142,143 In 2012, Queensland accounted for 65% (75/116) of notifications.

Figure 78: Notifications of leptospirosis, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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Age and sex distribution

The median age of leptospirosis notifications was 34 years (range 6–82 years) and 88% of cases (102/116) were male. The highest notification rate was observed in males in the 25–29 years age group (2.1 per 100,000 male population).

Typing information

The WHO/FAO/OIE Collaborating Centre for Reference and Research on Leptospirosis routinely conducts polymerase chain reaction-based serotyping for leptospirosis cases from Queensland (from whence the majority of cases are reported), and collates national data that may be submitted to the laboratory from other states or territories. At the time of compiling this report, data for 2012 were not publicly available.

Typing information from NNDSS was available for 84% (97/116) of notifications. Of those with typing information, the most common serovar was Arborea (23%, 22/97), followed by Hardjo (22%, 21/97), Australis (20%, 19/97) and Zanoni (20%, 19/97).

Ornithosis

Ornithosis (or psittacosis) is caused by infection with the bacterium Chlamydophila psittaci. It is transmitted to humans primarily from infected parrots of many species, but also poultry and a range of other birds.¹⁴⁴ Transmission to humans can occur via the inhalation of contaminated dried faeces, nasal or eye secretions and dust from the feathers. Individuals at risk of contracting ornithosis include bird owners and those with occupational exposure to birds.¹⁴⁵

Epidemiological situation in 2012

In 2012, there were 75 notified cases of ornithosis in Australia (a rate of 0.3 per 100,000), compared with the 5-year mean of 82 notifications (2007–2011). The majority of notifications in 2012 were from Victoria (63%, 47/75), this is a decrease compared with the number reported in 2011 (n=58)¹⁴⁶ (Figure 79).

Figure 79: Notifications of ornithosis, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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Just over half (51%, 24/47) of the 2012 Victorian cases were notified in the last quarter, with 15 notified in October. Following an increase in notified cases (n=7) in the Yarra Ranges Shire in Victoria during the 4th quarter, the Victorian Department of Primary Industries investigated a bird feeding area in the Dandenong Ranges, with reports of sick and dying birds in the area. The public health actions taken include supplying an information leaflet on ornithosis with packets of bird seed sold and logging the number of sick and dying birds surrendered to the Parks Victoria staff.¹⁴⁷

Age and sex distribution

The median age of ornithosis notifications was 55 years (range 30–79 years) and 56% (42/75) of notified cases were male.

Q fever

Q fever is caused by infection with the bacterium, Coxiella burnetii. The primary reservoirs of these bacteria are cattle, sheep and goats. C. burnetii is resistant to environmental conditions and many common disinfectants.¹⁴⁸ Q fever is most commonly transmitted via the airborne route, where the organism is carried in dust contaminated with tissue, birth fluids or excreta from infected animals.¹⁴⁹ Prior to the commencement of vaccination programs in Australia, approximately half of all cases in New South Wales, Queensland and Victoria were among abattoir workers.^150,151

The Australian Government funded the National Q Fever Management Program (NQFMP) between 2001 and 2006 for states and territories to provide free vaccine to at-risk groups (such as abattoir workers).¹⁵²

Adults at risk of Q fever infection, including abattoir workers, farmers, veterinarians, stockyard workers, shearers and animal transporters should be considered for vaccination. The administration of the Q fever vaccine requires a pre-vaccination screening test to exclude those recipients with a previous (unrecognised) exposure to the organism. A Q fever vaccine may cause an adverse reaction in a person who has already been exposed to the bacterium. Vaccination is not recommended for children under 15 years of age.²⁰

Epidemiological situation in 2012

In 2012, there were 358 notified cases of Q fever in Australia (a rate of 1.6 per 100,000), compared with the 5-year mean of 365 notifications (2007–2011).

Between 1991 and 2001, and prior to the introduction of the NQFMP, Q fever notification rates ranged from between 2.5 and 4.9 per 100,000.¹⁵² In 2012, the highest notification rate was in Queensland (4.2 per 100,000, n=192). Cases were reported in all jurisdictions except the Australian Capital Territory and Tasmania (Figure 80).

Figure 80: Notifications of Q fever, Australia, 2007 to 2012, by month and year of diagnosis and state or territory

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Age and sex distribution

The median age of Q fever notifications was 48 years (range 8–82 years) and 78% of cases (279/358) were male. The highest notification rate was observed in males in the 55–59 years age group (5.2 per 100,000 male population).

Tularaemia

Tularaemia is caused by infection with the bacterium Francisella tularensis. The most common modes of transmission are through arthropod bites, handling infected animals, inhalation of infectious aerosols or exposure to contaminated food or water. Small mammals such as rodents, rabbits and hares are often the reservoir.¹⁵³

Tularaemia was last notified in 2011, with 2 cases from Tasmania.³³ This was the first time that F. tularensis type B had been detected in the Southern Hemisphere.^154,155

Epidemiological situation in 2012

In 2012, there were no notified cases of Tularaemia in Australia.

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Other bacterial infections

Surveillance objectives

Other bacterial diseases in the national notifiable disease list are legionellosis, leprosy, invasive meningococcal disease and tuberculosis.

In 2012, there were 1,924 cases of other bacterial diseases notified to the NNDSS, representing less than 1% of all reported cases and a 4% decrease compared with 2011 (n=2,006).

Common objectives for the surveillance of diseases in this section are to monitor their epidemiology and to identify risk groups to accurately target control strategies.

Legionellosis

Legionellosis, caused by the bacterium Legionella, can take the form of either Legionnaires’ disease, a severe form of infection of the lungs or Pontiac fever, a milder influenza-like illness. The species most commonly associated with human disease in Australia are Legionella pneumophila and Legionella longbeachae. Legionella bacteria are found naturally in low levels in the environment. In the absence of effective environmental treatment Legionella organisms can grow to high numbers in air conditioning cooling towers, hot water systems, showerheads, spa pools, fountains or potting mix.

Epidemiological situation in 2012

A total of 382 cases of legionellosis were notified in 2012, representing a rate of 1.7 per 100,000. Compared with 2011 the overall number of legionellosis cases increased in 2012 by 7%. This was the highest since 2007 (Figure 81).

Figure 81: Notifications of legionellosis, Australia, 2007 to 2012, by year of diagnosis and species

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Data on the causative species were available for 93% (n=355) of notifications in 2012. Of the notifications with a reported species, proportionally there were slightly more cases of L. longbeachae (54%) than L. pneumophila (46%). There was a single confirmed case of L. micdadei. Serogroup data were available for 121 (74%) of the 163 L. pneumophila cases. Of these, 119 (98%) were due to serogroup 1 and the remainder were serogroup 2.

From 2007 to 2012, the annual number of notifications of L. longbeachae ranged from 136 to 190 cases and for L. pneumophila from 101 to 169 cases (Figure 81). In 2012, when compared with 2011, the number of cases of L. pneumophila decreased by 4% whilst case numbers of L. longbeachae increased by 11%.

Mortality data were available for 66% (n=252) of notifications in 2012 and of those, there were 11 deaths reported due to legionellosis. Most of these deaths were attributed to L. pneumophila (82%, n=9) (Table 24).

Table 24: Notifications of legionellosis, Australia, 2011, by species and state or territory

Species	State or territory								Aust.	Deaths due to legionellosis
	ACT	NSW	NT	Qld	SA	Tas.	Vic.	WA
L. longbeachae	1	29	3	37	26	5	16	73	190	2
L. pneumophila	0	64	0	23	13	6	45	12	163	9
L. micdadei	0	0	0	0	0	0	1	0	1	0
L. micdadei or pneumophila	0	0	0	0	0	1	0	0	1	0
Unknown species	1	9	0	10	0	0	7	0	27	0
Total	2	102	3	70	39	12	69	85	382	11
Rate (per 100,000 population)	0.5	1.4	1.3	1.5	2.4	2.3	1.2	3.5	1.7

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Geographical distribution

In 2012, rates of legionellosis varied from 0.5 per 100,000 in the Australian Capital Territory to 3.5 per 100,000 in Western Australia (Table 24). In 2012, the geographical distribution of L. longbeachae and L. pneumophila across jurisdictions mirrored that in 2011, with the exception of Queensland. The majority of notifications in South Australia, Queensland and Western Australia were attributed to L. longbeachae, whilst in New South Wales and Victoria L. pneumophila was the most common infecting species.

Age and sex distribution

In 2012, legionellosis was predominantly seen in older males. Overall, males accounted for the majority (61%) of the notifications with a male to female ratio of 1.6:1. There were no notifications in people under the age of 15 years. The age group with the highest notification rate was the 85 years or over group (7.5 per 100,000). The highest age and sex specific rates were observed in men aged 85 years or over (10.7 per 100,000, 16 notifications) and women aged 74–79 years (5.9 per 100,000, n=18) (Figure 82).

The 11 cases that were reported to have died due to legionellosis ranged in age from 38–87 years (median 70 years); 9 deaths were males and 2 were female. The majority of legionellosis notifications were in people aged 40 years or over (Figure 82).

Figure 82: Notification rate of legionellosis, Australia, 2012, by age group and sex

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Seasonality

In 2012, diagnoses of legionellosis (all species) were highest in July, with 46 cases notified in that month (Figure 83). L. pneumophila occurred most frequently in the summer months, with the highest number of notifications being recorded in February (n=21). L. longbeachae cases occurred most frequently in the spring months. However, the highest number of L. longbeachae cases reported in any 1 month occurred in July (n=26) of which half (n=13) were notified in Western Australia.

Figure 83: Notifications of legionellosis, Australia, 2007 to 2012, by month and year of diagnosis and species

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The seasonal pattern of L. longbeachae in 2012 reflected the seasonal pattern observed for this species over the previous 5 years, with the exception of 2009 when L. longbeachae occurred more frequently in the winter months. The seasonal pattern of L. pneumophila differed from the seasonal pattern observed for this species over the previous 4 years, with L. pneumophila occurring more frequently over the summer months as opposed to the autumn months. In 2007, L. pneumophila occurred more frequently in the summer months (Figure 83).

Place of acquisition

Place of acquisition was reported for 73% (n=280) of legionellosis notifications in 2012. Of these, 96% (n=267) were reported to have been acquired in Australia and 4% (n=13) overseas. Indonesia (n=3) and Thailand (n=2) were the most commonly reported places of acquisition for infections acquired overseas.

Outbreaks and clusters

In 2012, there were 5 L. pneumophila clusters and 1 outbreak of L. pneumophila notified to the NNDSS. Two clusters were reported in New South Wales and one each in Queensland, Victoria and South Australia with an outbreak reported in Victoria.

In New South Wales, 14 legionellosis notifications due to L. pneumophila serogroup 1 were reported from February to April in the Western Sydney and Nepean Blue Mountains Local Health Districts. This was approximately twice the number of cases usually seen in this period. The cases were clustered in 3 time periods; early February, mid-March and late April. Extensive investigations into these clusters were unable to determine any common sources for the infections.¹⁵⁶ An additional cluster in New South Wales was identified in November and December with 4 notified cases, but no common source was identified. One cluster and 1 outbreak were reported in Victoria in 2012, involving a total of 7 cases from the Northern and Western Metropolitan region. Both investigations were unable to definitively identify the source of infection.¹⁵⁷

The Queensland cluster consisted of 2 cases diagnosed in January and February of 2012. The cases were identified in residents of a retirement village in South East Queensland. An environmental investigation of the facility was undertaken with water samples collected from the spa, pool and resident showers. The water samples were negative for L. pnuemophila and no source of the infection was identified.

The cluster in South Australia formed part of an investigation that was conducted from January to March 2013. In total, there were 13 cases identified as the same cluster with 3 cases from South Australia and 3 cases from Victoria.

Change in the epidemiology of species from 1991 to 2012

Since 1991, the number of legionellosis notifications has continued to rise (Figure 84). Before 1998, legionellosis notifications were more likely to be attributed to L. pneumophila. However, since 1998, the most common infective species has alternated between L. pneumophila and L. longbeachae.

Figure 84: Notifications of legionellosis, Australia, 1991 to 2012, by year of diagnosis and species

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Discussion

Since reporting began in 1991, the number of notifications reported annually for legionellosis has increased by two-thirds from 122 notifications in 1991 to 382 notifications in 2012. The increased use of more sensitive diagnostic testing may have contributed to this rise in notifications.

The demographic profile of legionellosis cases since 1991 has remained consistent with the recognised epidemiology of the disease.^158–160 Less than 7% of notified cases are in persons under the age of 30 years or over 70% are in those aged 50 years or over. However, since reporting began in 1991 there has been a change in the predominant notified species. Whilst L. pnuemophila was the predominate species notified between 1991 and 1997, since 1998 (with the exception of the 2000 L. pneumophila outbreak) the most commonly reported species of Legionella has alternated between L. pnuemophila and L. longbeachae.

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Leprosy

Leprosy is a chronic infection of the skin and peripheral nerves due to the bacterium Mycobacterium leprae. Leprosy is an uncommon disease in Australia, although, a very small number of people are diagnosed each year, with the majority of cases acquiring the infection overseas. The incidence of leprosy worldwide is declining due to various factors including economic development, the use of Bacillus Calmette–Guérin vaccine and high coverage with multi-drug therapy.¹⁹ Leprosy is not highly infectious. People at risk are generally in close and frequent contact with leprosy patients or living in countries where the disease is more common. The disease is curable and once a person with leprosy begins appropriate treatment, they quickly become non-infectious.

Epidemiological situation in 2012

There were 4 notifications of leprosy in 2012, representing a rate of 0.02 per 100,000.

All cases were residents of Victoria and were reported as being non-Indigenous. Cases ranged from 29–72 years of age. In 2012, 2 cases were male and 2 female. All four of these cases were reported as having acquired leprosy overseas.

The number of leprosy cases decreased in 2012 by half, from the 8 cases reported in 2011 (Figure 85). Since 1992, the annual number of notifications of leprosy has ranged from 4 to 19 cases.

Figure 85: Notifications of leprosy, Australia, 1992 to 2012, by year of diagnosis and Indigenous status

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Meningococcal disease (invasive)

Meningococcal disease is caused by the bacterium Neisseria meningiditis. Invasive disease occurs when bacteria infect a normally sterile site, usually the blood (septicaemia), cerebrospinal fluid (meningitis) or both. Asymptomatic respiratory tract carriage of meningococci occurs in 5%–10% of the population and prevalence may be higher when groups of people occupy small areas of any space.^19,20 The disease is transmitted via respiratory droplets and has an incubation period of between 1 and 10 days, most commonly 3 to 4 days.^20,161 Infection occasionally causes a rapidly progressive serious illness, most commonly in previously healthy children and young adults. Globally, serogroups A, B, C, W135 and Y most commonly cause disease.¹⁹ Historically, N. meningitidis serogroups B and C have been the major cause of IMD in Australia.

Since 2003, meningococcal C vaccine has been available for those 12 months of age as part of the childhood immunisation schedule funded under the NIP. Additionally, a catch-up program provided access to the meningococcal C vaccine for children and adolescents born between 1984 and 2001. There was a staged implementation, ending in 2006, with a funded vaccine made available through general practitioners for the 1–5 years age group and through school based clinics for the 6–19 years age group.

Epidemiological situation in 2012

In 2012, there were 223 cases of IMD, representing a rate of 1.0 per 100,000. This was a decrease of 8% on the cases notified in 2011 (n=241) and the lowest number of cases notified annually compared with the preceding 10 years (Figure 86).

Figure 86: Notifications of invasive meningococcal disease, Australia, 2002 to 2012, by year of diagnosis and serogroup

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Most cases (n=219) notified in 2012 met the definition for a confirmed case, that is, diagnosed based on laboratory definitive evidence, or laboratory suggestive evidence and clinical evidence.¹⁶² A small number of cases (n=4) met the definition for a probable case, that is, diagnosed based on clinical evidence only.

Data on serogroup were available for 89% of cases in 2012. Seventy-four per cent of cases were due to serogroup B, 7% serogroup Y, 5% serogroup C and 3% serogroup W135. The number of cases of IMD caused by serogroup B notified in 2012 was the lowest compared with the number of cases notified annually in the preceding 10 years. Notifications of IMD caused by serogroup C organisms have decreased substantially since the introduction of the meningococcal C vaccine on the NIP in 2003, with fewer than 25 cases reported annually. Notifications of IMD caused by serogroup Y peaked in 2012 with 15 cases, which was the highest number of cases reported annually compared with the preceding 10 years.

Mortality data were available for 60% (n=133) of cases reported to the NNDSS in 2012. Twelve cases were reported as having died from IMD; 10 due to serogroup B and 2 due to serogroup C (Table 25). Of the deaths due to serogroup B, five were children aged less than 2 years, two were young adults and the remaining three were adults aged over 25 years. Of the 2 serogroup C related deaths, one occurred in an unvaccinated person in the 15–19 years age group, who was eligible for vaccination. The second death was an infant too young for vaccination.

Of the 11 cases of IMD due to serogroup C in 2012, four were aged between 1 and 29 years and therefore would have been eligible for vaccination either through routine childhood immunisation or under the meningococcal C catch up program. All four of these cases were reported as not vaccinated with meningococcal C vaccine.

Geographical distribution

All jurisdictions reported in accordance with the national case definition for IMD, except the Australian Capital Territory and New South Wales where conjunctival cases were also reported. Conjunctival cases cannot be distinguished from invasive cases in the national dataset.

In 2012, cases of IMD were reported from all states and territories, ranging from 1 case from the Australian Capital Territory to 66 from New South Wales (Table 25). Notification rates ranged from 0.3 per 100,000 in the Australian Capital Territory to 1.8 per 100,000 in South Australia.

Table 25: Notifications of invasive meningococcal disease and deaths due to invasive meningococcal disease, Australia, 2012, by serogroup and state or territory

Age and sex distribution

More males than females were reported with IMD in 2012, with a male to female ratio of 1:0.8. Two-thirds of cases (n=147) were less than 25 years of age, of which those less than 5 years of age made up almost half (n=70). Cases aged less than 5 years had the highest age-specific rate at 4.7 cases per 100,000. High rates also occurred among the 15–19 years age group (2.2 per 100,000) followed by the 20–24 years age group (1.6 per 100,000) (Figure 87).

Figure 87: Notification rates of invasive meningococcal disease, Australia, 2012, by age and sex

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Serogroup B accounted for the majority of cases across all age groups including those aged less than 25 years, where it accounted for 85% of cases with serogroup information available. While the age-specific rates of serogroup B infection in 2012 remain high compared with other serogroups, they continue to trend downward across all age groups (Figure 88).

Figure 88: Notification rate for serogroup B invasive meningococcal disease, Australia, 2007 to 2012, by selected age groups

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Of the 11 cases of IMD due to serogroup C notified in 2012 only 4 were among children and young adults aged less than 25 years of age. While there was an increase in the rate of IMD due to serogroup C in the 15–19 years and 20–24 years age groups, age-specific rates have been maintained at very low levels, with no age group exceeding 0.2 cases per 100,000 in 2012 (Figure 89).

Figure 89: Notification rate for serogroup C invasive meningococcal disease, Australia, 2007 to 2012, by selected age group

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Seasonality

An average of 17 cases of IMD was reported each month in 2012, with a range of 5–30 cases per month. A clear seasonal pattern was apparent, with the highest number of notifications reported in the winter months, which is consistent with the normal seasonal pattern for this disease (Figure 90). The seasonal trend was more marked in cases aged 5 years or over.

Figure 90: Notifications of invasive meningococcal disease, Australia, 2007 to 2012, by age group and month and year of diagnosis

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Vaccination

Coverage of the meningococcal C vaccine has remained at high levels since its introduction, with the latest data indicating that in 2010 almost 94% of Australian children were immunised by 24 months of age.¹⁶³

Laboratory based meningococcal disease surveillance

The Australian Meningococcal Surveillance Program (AMSP) was established in 1994 for the purpose of monitoring and analysing isolates of N. meningitidis from cases of IMD in Australia. The program is undertaken by a network of reference laboratories in each state and territory, using standardised methodology to determine the phenotype (serogroup, serotype and serosubtype) and the susceptibility of N. meningitidis to a core group of antibiotics.

Annual reports of the AMSP are published in CDI. The 2012 data from AMSP showed that 82% of isolates tested demonstrated decreased susceptibility to the penicillin group of antibiotics, and just 1 isolate exhibited resistance to penicillin.⁴¹ While all isolates remained susceptible to third generation cephalosporins and ciprofloxacin, a small number of isolates were reported with an altered susceptibility to rifampicin.

Discussion

In Australia in 2012, IMD has reached its lowest level since national notifications began in 1991. This reduction has been seen most markedly with disease due to serogroup C. However, declines in disease caused by serogroup B are also evident. The slight increase in disease incidence caused by serogroup Y organisms should be closely monitored to determine whether this is an increasing trend.

Tuberculosis

TB is an infection predominantly caused by the bacterium Mycobacterium tuberculosis. It is transmitted by airborne droplets produced by people with pulmonary TB during coughing or sneezing. About one-third of the world’s population has latent TB infection, which means people have been infected with TB bacteria but are not ill with disease and cannot transmit it. Generally healthy people infected with TB bacteria have a 10% lifetime risk of progressing to disease. However, persons with a compromised immune system, such as those living with HIV, suffering from malnutrition or diabetes, or people who use tobacco, have a much higher risk of falling ill.¹⁶⁴

While Australia has one of the lowest rates of TB in the world, the disease remains a public health issue. Further analyses, including the identification of risk groups and reporting on treatment outcomes, are reported in the TB annual reports also published in CDI.¹⁶⁵

Epidemiological situation in 2012

In 2012, a total of 1,315 cases of TB were notified to the NNDSS, representing a rate of 5.8 per 100,000. This was similar to the number of cases reported in the previous year (n=1,399). While the substantial decline in the rate of TB since the 1960s has been maintained, notification rates in the last decade have tended to increase, with the previous 3 years exceeding 6 cases per 100,000 (Figure 91).

Figure 91: Notification rate for tuberculosis, Australia, 1960 to 2012

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Geographical distribution

New South Wales (n=467), Victoria (n= 366), Queensland (n=176) and Western Australia (n=172) accounted for 90% of all cases of TB diagnosed in Australia. Notification rates were highest in the Northern Territory (11.9 per 100,000), Western Australia (7.1 per 100,000), Victoria (6.5 per 100,000) and New South Wales (6.4 per 100,000). Rates in the remaining jurisdictions were all lower than the national notification rate of 5.8 per 100,000.

Age and sex distribution

In 2012, TB was predominantly seen in young adults and older males. Males accounted for more than half (55%) of the notifications of TB, resulting in a male to female ratio of 1.2:1. The age group with the highest notification rate was the 25–29 years age group (15.0 per 100,000). The highest age and sex specific rates were observed for men aged 85 years or over (16.1 per 100,000) and in women aged 25–29 years (15.1 per 100,000) (Figure 92).

Figure 92: Notification rate for tuberculosis, Australia, 2012, by age group and sex

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