​​​ On this page

Refugee health

A summary of the 7 November 2014 Bug Breakfast forum

Genevieve Whitlam, Public Health Officer Trainee, NSW Ministry of Health
Dr Mitchell Smith, Director, NSW Refugee Health Service
Associate Professor Ben Marais, Paediatrics & Child Health, Children’s Hospital, Westmead & The Marie Bashir Institute for Infectious Diseases and Biosecurity


A refugee is a person who “owing to a well-founded fear of being persecuted for reasons of race, religion, nationality, membership of a particular social group or political opinion, is outside the country of his nationality, and is unable to, or owing to such fear, is unwilling to avail himself of the protection of that country”.[1] In the last 10 years, Australia has settled on average between 12,000 and 14,000 refugees each year.[2,3] This article provides an overview of the factors contributing to the high disease burden in the resettled refugee population, the prevalence of various diseases, efforts to promote the health of refugees upon arrival and strategies to minimise public health risk to Australian citizens.

Humanitarian program

Australia’s humanitarian program is comprised of two components:

  1. Offshore resettlement: people who have been granted refugee status overseas (including Woman at Risk visas) and the Special Humanitarian Program (for those sponsored by family or an organisation);
  2. Onshore protection: people who apply for refugee status while already in Australia (who may have arrived with or without a visa).

In 2014-15, 13,756 visas were granted under the Australian Humanitarian Program. The majority (11,009) of these were offshore component visas including 6,002 Refugee stream visas (of which 1,009 were granted to Woman at Risk visa applicants) and 5,007 Special Humanitarian Program visas).[3] The most common countries of birth for offshore visa grants were Iraq (21%), Syria (20%) and Burma (Myanmar) (18%).[3] Around one-third of Australia’s Humanitarian arrivals settle in NSW, with over half of the arrivals in 2014-15 residing in Fairfield (38%) or Liverpool (15%) Local Government Areas.[3]

Pre-departure context and health screening

Exposure to political and social unrest, human rights abuses, poor environmental conditions and limited access to health care all contribute to poor health. Many displaced persons spend considerable periods of time in refugee camps with multiple environmental risk factors. Others live in the community in neighbouring countries where they may be victimised, and access to basic amenities and health care is limited. Table 1 lists common environmental risk factors within refugee camps and some of the associated infectious disease risks.

Table 1: Environmental risk factors and infectious diseases in refugee camps [5-8].

Environmental risk factorsInfectious diseases

Contaminated food and water

Inadequate sanitation

  • Viral diarrhoea
  • Shigella dysentery
  • Hepatitis A and E
  • Cholera
  • Polio
  • Intestinal parasites (e.g. Giardiasis)
Overcrowded and sub-standard housing
  • Vector-borne disease (e.g. malaria, dengue)
  • Tuberculosis
  • Respiratory infections
  • Measles
  • Meningococcal meningitis
  • Diphtheria

Australia has a strict health assessment process for refugees and other humanitarian entrants, that mirrors the process for all migrants to Australia, to minimise public health and safety risks to the Australian community.9 A detailed visa applicant medical examination, including a full medical history and examination, urinalysis (if ≥5 years), chest x-ray (if ≥11 years) and HIV test (if ≥15 years), occurs 3 to 12 months before travel. An additional Departure Health Check occurs, for funded refugees within 72 hours of departure - this aims to determine fitness to fly, and provides pre-departure interventions such as treatment for intestinal parasites, measles, mumps and rubella (MMR) immunisation, and rapid malaria testing where relevant.9 For the recent refugee cohort ex-Syria, the Australia Government has introduced hepatitis B testing. Latent tuberculosis (TB) infection screening is now being performed in refugees and migrants aged 2 to 10 years from countries with a TB incidence of greater than 40/100,000.

Prevalence of disease in newly arrived refugees

Prevalence estimates of various infectious diseases in the resettled refugee population in Australia can vary considerably. Much of this variation is driven by the changing international political situation and conflict zones that determine the regions of the world from which refugees are fleeing. Previous studies within Australia of resettled refugees report prevalence estimates to range between 5–27% for schistosomiasis10-11, 2–5.7% for strongyloidiasis10¬-11, 0.5–16% for malaria10-13, 0–5%10-11, 13 for syphilis. Changes to the Australian Government’s overseas screening policies can influence these data over time – for example, malaria is now rare in newly arrived refugees since the Departure Health Check was introduced in 2005, and syphilis screening is now being done routinely in those 15 years and above. Gastrointestinal infections and parasites tend to be more prevalent in populations resettling from North and Sub-Saharan Africa.[10] Chronic hepatitis B infection is ubiquitous in many regions, being reported in 4 to 7% of refugees arriving from North and sub-Saharan Africa as well as South and Southeast Asia.[10]

Of refugees who arrived in Sydney in 2013 and 2014 and who were tested, 4% were positive for strongyloides and 1% for syphilis. The overall prevalence of chronic hepatitis B was 1.7%. However, the prevalence was much higher in refugees from Myanmar and Tibet/India (11% and 13% respectively). About 66% were non-immune to hepatitis B. During this period, the majority of arrivals were from the Middle East.[14]

Pre-departure screening of intending migrants and refugees for TB identifies individuals with active TB and requires them to complete TB treatment and confirm cure before travel to Australia. Those with evidence of latent M. tuberculosis infection or a past history of TB are required to attend a chest clinic upon arrival, as part of a special TB Health Undertaking. The proportion of newly arrived refugees with evidence of M. tuberculosis infection (a positive tuberculin skin test) varies between 18-25%.[10-13] This is relevant for monitoring and control purposes as most TB disease resulting from past infection occurs within the first 5 years after migration, although re-exposure may occur with repeat visits to TB endemic countries.[15]

Public health response

There are a variety of Government and non-Government organisations whose role is to provide specialised health and wellbeing services to newly arrived refugees and other migrants.16 Relevant Local Health Districts provide clinical services for refugees such as nurse-led screening and specialised paediatric clinics, as well as health education and health promotion, training and support to health professionals, policy and planning advice and research. Medicare provides item numbers for General Practitioners who perform health assessments for humanitarian entrants.[9]

In response to the Ebola Virus outbreak in West Africa, NSW implemented additional public health measures in line with National Guidelines to identify and respond to suspected Ebola cases and minimise the risk of transmission to health care workers and the general population within Australia.[17] This included detailed guidelines and management in conjunction with enhanced surveillance for international arrivals from Ebola affected countries or those who had contact with an Ebola case in any country.


Many humanitarian arrivals have experienced traumatic life events and spent considerable time in refugee camps or marginalised communities where basic resources and services are lacking. This exposes them to multiple health risks including infectious diseases. Australia’s public health measures begin before arrival. During the initial settlement period, NSW's public health response continues with targeted screening and management of region specific infectious disease risks. The wide scope of the public health response and support systems is crucial to ensuring optimal refugee health as well as protection of the broader community.


  1. Office of the United Nations High Commissioner for Refugees 1951. Convention and Protocol Relating to the Status of Refugees. Viewed 30 June 2016 at UNHCR.
  2. Australian Government Department of Immigration and Border Protection. 2014. Historical Migration Statistics. Table 4.1 Humanitarian Programme visa grants, 1977-78 to 2012-13.
  3. Australian Government Department of Immigration and Border Protection. Fact Sheet – Australia’s Refugee and Humanitarian Programme. Viewed 30 June 2016.
  4. Australian Government Department of Social Services. Table created using Settlement Reporting Facility on 30 June 2016.
  5. Ahmed JA, Moturi E, Spiegel P, Schilperoord M, Burton W et al. 2013. Hepatitis E Outbreak, Dadaab Refugee Camp, Kenya, 2012. Emerging Infectious Diseases; 19 (6): 1010-1011.
  6. Mahamud AS, Ahmed JA, Nyoka R, Auko E, Kahi V et al. 2012. Epidemic cholera in Kakuma Refugee Camp. Kenya, 2009: the importance of sanitation and soap. Journal of Infection in Developing Countries; 6 (3): 234 – 241.
  7. Hershey CL, Doocy S, Anderson J, Haskew C, Spiegel P et al. 2011. Incidence and risk factors for malaria, pneumonia and diarrhea in children under 5 in UNHCR refugee camps: a retrospective study. Conflict and Health; 5: 24. Viewed 30 June 2016 at www.conflictandhealth.com/content/5/1/24.
  8. Wisner B and Adams J (Ed.) 2003. Environmental health in emergencies and disasters: a practical guide. Chapter 11 Control of communicable diseases and prevention of epidemics. World Health Organization: Geneva. Viewed 30 June 2016 at http://apps.who.int/iris/bitstream/10665/42561/1/9241545410_eng.pdf
  9. Australian Government Department of Health 2014. Health assessment for refugees and other humanitarian entrants into Australia. Viewed 30 June 2016 at www.health.gov.au/internet/main/publishing.nsf/Content/mbsprimarycare_mbsitem_refugees_qanda.
  10. Martin JA & Mak DB 2006. Changing faces: a review of infectious disease screening of refugees by the Migrant Health Unit, Western Australia in 2003 and 2004. Medical Journal of Australia; 185: 607-610.
  11. Johnstone V, Smith L & Roydhouse H. 2011. The health of newly arrived refugees to the Top End of Australia: results of a clinical audit at the Darwin Refugee Health Service. Australian Journal of Primary Health. Viewed 30 June 2016 at http://dx.doi.org/10.1071/PY11065.
  12. Raman S, Wood N, Webber M, Taylor K & Isaacs D. 2009. Matching health needs of refugee children with services: how big is the gap? Australia and New Zealand Journal of Public Health; 33 (5): 466-470.
  13. Sheikh M, Pal A, Wang S, MacIntyre CR, Wood NJ, Isaacs D et al. 2009. The epidemiology of health conditions of newly arrived refugee children: a review of patients attending a specialist health clinic in Sydney. Journal of Paediatrics and Child Health; 45: 509-513.
  14. NSW Refugee Health Service 2014. Unpublished data.
  15. Frothingham R, Stout JE, Hamilton CD. 2005. Current issues in global tuberculosis control. International Journal of Infectious Diseases; 9: 297-311.
  16. NSW Multicultural Health Communication Service. NSW Multicultural Health Services Directory. Viewed on 30 June 2016 at www.mhcs.health.nsw.gov.au/policiesandguidelines/supportinfo/pdf/nsw-multicultural-health-services-directory.
  17. NSW Ministry of Health 2014. Ebola Virus Disease. Viewed 30 June 2016 at www.health.nsw.gov.au/Infectious/controlguideline/Pages/ebola-virus.aspx.

Healthcare-associated infections

A summary of the 6 March 2015 Bug Breakfast forum

Damien Cordery, Public Health Training Program, NSW Ministry of Health


Healthcare-associated infections (HAI) are any infection that is contracted or develops during the treatment for other conditions in a healthcare setting. HAI are generally associated with hospitals but can occur in any healthcare setting. In Australia there are around 200,000 HAI in acute care facilities each year (NHMRC, 2010). This makes HAI the most common complication affecting patients in hospital.

HAI have significant consequences for the patient and the health system. HAI increase morbidity and mortality and increase the length of stay for patients. Impacts on the health system primarily involve an increased cost of care, related to greater complexity of care and the requirement for extensive infection control activities, during both prevention and patient management.

The National Health and Medical Research Council recommends transmission precautions for over 140 conditions. However, the pathogens of greatest concern in the healthcare setting are the antibiotic resistant organisms.


Several categories of patient are more susceptible to HAI than others. These include:

  • older patients
  • those with compromised immunity
  • those with comorbidities (e.g. diabetes)
  • those with wounds or invasive devices


Transmission of pathogens is dependent on the specific organism. Modes of transmission with examples of pathogens spread by each mode are provided in Table 1.

Table 1: Mode of transmission and examples of potential pathogens

Transmission methodPathogens


  • Direct (person to person)
  • Indirect (via equipment/environment)
  • Clostridium difficile
  • Norovirus
  • Influenza
  • Pertussis
  • Measles
  • Tuberculosis

Other modes of transmission may involve the use of devices or equipment such as intravascular lines, haemodialysis access and urinary catheters.


The main infection control methods for preventing the transmission of HAI include:

  • training and enforcement of hand hygiene
  • appropriate use of personal protective equipment
  • environmental cleaning
  • isolation of infected patients (in either single patient rooms or HAI positive patients together).

Hand hygiene is seen as particularly important. Hand hygiene compliance has been increasing since 2010, with NSW compliance rates consistently above the national average (Figure 1).

Figure 1: Hand hygiene compliance rates

Since April 2010, compliance with hand hygiene has been steadily improved in NSW from 61.8% to 83.0%; it has also improved across the country. Link to data table follows image.
Text alternative
Source: CEC, Hand Hygiene Program

Antibiotic resistance

Pathogens that develop antibiotic resistance and become established in healthcare facilities tend to share a number of characteristics. Firstly, they tend to survive well on surfaces, potentially for days to weeks, meaning that there is good capacity for indirect transmission. These organisms can also colonise individuals (patients, staff or visitors) which creates the potential for colonised individuals to pass pathogens to susceptible patients, or colonised patients to develop infections when they are admitted to hospital.

The resistant organisms of greatest concern are Methicillin-Resistant Staphylococcus aureus (MRSA), Vancomycin-Resistant Enterococci and Multi-Resistant Gram-Negative which can include E.coli, Klebsiella and Salmonella species.

Case study

A novel strain of MRSA was identified in a Local Health District in NSW in 2013. A case control study demonstrated that the novel strain did not result in significantly different morbidity and mortality than other circulating MRSA strains. Whole Genome Sequencing (WGS) was carried out on the available strains in an effort to better define transmission pathways during the outbreak. Although the analysis is ongoing, the additional information provided by WGS demonstrates the utility of this method in clarifying the relationship between isolates that may not otherwise be definitively linked.


HAI are an ongoing concern as they contribute to increased morbidity and mortality and result in increased cost of healthcare. Improvements in isolate typing (strain identification and whole genome sequencing) may lead to improved definition of transmission pathways and more efficient infection control.


NHMRC (2010), Australian Guidelines for the Prevention and Control of Infection in Healthcare. Commonwealth of Australia.

Locally acquired hepatitis E in NSW

A summary of the 6 February 2015 Bug Breakfast forum

Simon Willcox, Trainee Public Health Officer, Health Protection NSW
Catriona Furlong, Epidemiologist, OzFoodNet, Health Protection NSW

Hepatitis E virus (HEV) is a single strand RNA virus that was first discovered in the 1980s (1). There are four major genotypes recognised in mammalian HEV.

Signs and symptoms

Typical signs and symptoms of HEV are indistinguishable from those experienced during any other acute phase of hepatic illness and include jaundice, abdominal pain, anorexia, nausea, vomiting, fever, pale stools, dark urine, and an enlarged, tender liver.[2]

On rare occasions HEV can cause fulminant hepatitis (acute liver failure), leading to death.

In genotypes 1 and 2, fulminant hepatitis occurs more frequently during pregnancy with a mortality rate of up to 25 per cent.[1]

Asymptomatic infection is common.

Incubation period

The incubation period for HEV is 15 to 64 days, with a mean of 26-42 days.[2]

The period of communicability is unknown.


For genotypes 1 and 2, symptomatic infection is most common in young adults aged 15 to 35 years.[1]

For genotypes 3 and 4, symptomatic infection is most common in elderly men.[1]

Chronic HEV infection and reactivation of the virus have been reported in people who are immunocompromised.

Virus activity


Hepatitis E virus is probably the most common cause of acute viral hepatitis in the world and has a case fatality rate of 1-3%, higher during pregnancy.[1]

Genotypes 1 and 2 of HEV are prevalent across much of the developing world including Asia, Africa and Central America. In these areas HEV is transmitted primarily via the faecal-oral route through contaminated water systems, poor sanitation and weak public health systems. Genotypes 1 and 2 are a major source of sporadic and epidemic hepatitis in these regions.[1]

Genotype 3 is found in developed nations including Western Europe, USA, Japan and New Zealand. In these areas HEV causes sporadic disease and is zoonotic.[1]

Genotype 4 is found in China and Japan where it also causes sporadic disease and is zoonotic.

Seroprevalence rates (IgG positivity) vary across the world [1]:

  • 3% in Japan
  • 7% in Spain
  • 16% in South-west France and England [3]
  • 21% in USA.


Almost all notified cases of HEV in Australia have had a history of travel to an endemic region during their incubation period [4]. Nationally, there are between 15 – 45 notifications received per year. In NSW, there are between 10 – 20 notifications received per year and mostly in 20 – 60 year olds.

Figure 1: Number of Hepatitis E notifications in Australia by State and Territory from 2005 to 2014

Hepatitis E notifications in Australia by State and Territory from 2005 to 2014. The number of cases of hepatitis E notified in Australia has varied between 18 in 2007 and 56 in 2014. In 2014 most cases were notified in NSW. Link to data table follows image.
Text alternative
Data from Australian Government Department of Health National Notifiable Diseases Surveillance System. http://www9.health.gov.au/cda/source/rpt_4_sel.cfm Accessed: 4:20pm 24 July 2015

Figure 2: Hepatitis E notifications in Australia by age group and gender in 2014

Hepatitis E notifications in Australia by age group and gender in 2014. Notifications occured for ages 20-80 and were heighest in 30-34 year age group and lowest in 50-54, 70-74 and 75-79. Link to data tables follows image.
Text alternative

Information on locally acquired HEV in Australia is limited. The first case of locally acquired HEV infection was reported in the Northern Territory in 1995 (5). The source of infection was not determined. There were also two locally acquired cases notified in 2005, one in Victoria and the other in Queensland [4].

A cluster of locally acquired cases of HEV infection in New South Wales was investigated in 2014 [6]. Seventeen cases were linked to consuming pork liver pâté at a restaurant in NSW. The likely source of infection was consumption of undercooked pork liver. An additional seven people with locally acquired infections reported consuming a pork product during their incubation periods. HEV RNA was detected in 16 of these 24 cases, all genotype 3.

A study of HEV seroprevalence among a cohort of Australian blood donors was conducted in late 2013 [7]. This study found that 6 per cent of donors had evidence of prior HEV infection. The study demonstrated HEV exposure in travellers and non-travellers suggesting the possibility of both imported and locally acquired HEV in Australia.

Evidence for hepatitis E as a zoonosis

Internationally, the virus is highly prevalent in domestic pigs, wild boar and deer. Hepatitis E RNA has been found in animal stool and tissue – these may contain sufficient viral load to be infectious. There is high genetic sequence relatedness between animal and human genotype 3 isolates[1,8]. Significant zoonotic risk factors have been identified in human cases.

Internationally, Hep E infection is almost universal amongst pig herds [9]. There is a high RNA sequence similarity between human and swine Hep E sequences from the same geographical region [8]. Cross-sectional studies have found a significant association between occupational exposure to swine and infection with HEV [9].

In Australia, a study conducted in 1999 found HEV infection in pig herds in NSW, VIC and NT (30%-95% seroprevalence in commercial pigs, 17% wild pigs) [10].

There is some evidence for HEV as a pork related zoonosis [11]. HEV RNA was found in faeces, blood and livers of pigs of slaughtering age in several European studies [12,13,14]. HEV RNA found in about 1 in 20 pork livers in butcher shops in the Netherlands and Germany. Pork pies, liver pate, undercooked pork meat, homemade sausages and handling raw pig liver have been associated with HEV infection in various developed countries [15].

Treatment and prevention

There is no specific treatment for HEV infection which is usually self-limiting. Hospitalisation is generally not required; except for people with fulminant hepatitis or symptomatic pregnant women [2].

Key strategies for prevention:

  • provide clean drinking water
  • provide adequate sanitary infrastructure
  • adhere to safe food practices such as cooking meat thoroughly
  • implement good case diagnosis and surveillance
  • people working with animals must wear personal protective equipment.

The first vaccine to prevent Hepatitis E infection was registered in China in 2011 [16]. Although it is not available globally, it could potentially become available in a number of other countries.


There is evidence of locally acquired hepatitis E virus in New South Wales. Surveillance of this disease should continue and surveillance data will inform further actions to control this disease as required.


  1. Kamar, N., et al., Hepatitis E. The Lancet, 2012. 379(9835): p. 2477-2488.
  2. Heymann, D.L., Control of Communicable Diseases Manual. 20 ed. 2015, Washington DC, USA: American Public Health Association.
  3. Mansuy, J.M., et al., Seroprevalence in blood donors reveals widespread, multi-source exposure to hepatitis E virus, southern France, October 2011. Euro Surveill, 2015. 20(19).
  4. Owen, R., et al., Australia's notifiable diseases status, 2005: Annual report of the National Notifiable Diseases Surveillance System, A.G.D.o. Health, Editor. 2005: Online.
  5. Heath, T.C., J.N. Burrow, and B.J. Currie, Locally acquired hepatitis E in the Northern Territory of Australia. The Medical Journal of Australia. 162(6): p. 318-319.
  6. Yapa C.M., et al., First reported outbreak of locally acquired hepatitis E virus infection in Australia. The Medical Journal of Australia. 204(7):p. 274.
  7. Shrestha, A.C., et al., Hepatitis E virus and implications for blood supply safety, Australia. Emerging Infectious Diseases, 2014. 20(11): p. 1940-1942.
  8. McCreary, C., et al., Excretion of hepatitis E virus by pigs of different ages and its presence in slurry stores in the United Kingdom. The Veterinary Record, 2008. 163: p. 261-265.
  9. Lewis, H.C., O. Wichmann, and E. Duizer, Transmission routes and risk factors for autochthonous hepatitis E virus infection in Europe: a systematic review. Epidemiology and Infection, 2010. 138(2): p. 145-166.
  10. Chandler, J.D., et al., Serological evidence for swine hepatitis E virus infection in Australian pig herds. Veterinary Microbiology, 1999. 68: p. 95-105.
  11. Christou, L. and M. Kosmidou, Hepatitis E virus in the Western world - a pork-related zoonosis. Clinical Microbiology and Infection, 2013. 19: p. 600-604.
  12. Fernandez-Barredo, S., et al., Detection of hepatitis E virus shedding in feces of pigs at different stages of production using reverse transcription-polymerase chain reaction. Journal of Veterinary Diagnostic Investigation, 2006. 18: p. 462-465.
  13. Caprioli, A., et al., Detection of hepatitis E virus in Italian pig herds. The Veterinary Record, 2007: p. 423.
  14. Fernandez-Barredo, S., et al., Prevalence and genetic characterisation of hepatitis E virus in paired samples of feces and serum from naturally infected pigs. The Canadian Journal of Veterinary Research, 2007. 71: p. 236-240.
  15. Colson, P., et al., Pig liver sausage as a source of hepatitis E virus transmission to humans. The Journal of Infectious Diseases, 2010. 202(6): p. 825-834.
  16. Teshale, E. and J.W. Ward, Making hepatitis E a vaccine-preventable disease. The New England Journal of Medicine, 2015. 372(10): p. 899-901.


A summary of the 1 May 2015 Breakfast forum

Brooke Shepherd, Public Health Training Program, NSW Ministry of Health
Dr Tony Merritt, Public Health Physician, Hunter New England Population Health
Dr Paul Douglas, Chief Medical Officer & Assistant Secretary Immigration Health Branch, Department of Immigration and order Protection


Tuberculosis (TB) is a disease primarily caused by infection with Mycobacterium tuberculosis (MTB). It is transmitted through inhalation of droplets produced by an infected person through coughing, laughing, or sneezing. Most people are infected by close contacts, such as friends or family.

Latent TB infection refers to when TB is present in the body but is inactive. It does not cause any symptoms and can persist for a lifetime. Around 90% of people infected will always remain in this state while 10% go on to develop TB disease. [1].This is more likely to occur when the body's immune system is weakened due to serious illness, drug and alcohol misuse or HIV infection. TB can attack any part of the body but the lungs are the most common site. Symptoms can include prolonged cough illness, fevers, weight loss, night sweats, loss of appetite, and blood stained sputum. Progression from latent TB infection to TB disease can occur from weeks to decades after initial infection, but around half will occur in the first 2 years.

Diagnosis and treatment

Tests to diagnose TB include the tuberculin skin test (TST), primarily used to determine exposure to TB rather than TB disease and the Interferon Gamma Release Assay, measuring immune reaction to TB. Tests for TB disease include chest x-ray and sputum collection. Culture remains the definitive “gold standard” investigation for TB disease. It is highly specific but MTB is slow to grow. Microscopy and PCR are also commonly used as they are more rapid than culture. Despite these tests around 20% of TB cases each year in Australia are notified on the basis of clinical symptoms alone [2].

Latent TB infection can be managed through preventive therapy or monitoring with regular chest x-rays for detection of early disease. The use of preventive therapy for latent TB infection significantly decreases the likelihood of subsequent TB disease. However benefits need to be weighed against potential side effects, particularly in older patients and those less likely to progress to TB disease.

TB disease can be treated with a combination of first line antibiotics (isoniazid, rifampacin and others) lasting at least six months. To support compliance and monitor for drug effects, treatment is usually supervised (DOTS; Directly etc.) and if the course is completed this generally results in cure. There is currently around a 90% completion rate of treatment in NSW. Drug resistant strains of TB have been identified in Australia, and are managed through multidisciplinary teams with TB expertise [3].

Global and local context

TB is a disease of global public health significance. The World Health Organization estimates that one-third of the world’s population is infected with TB, with 9 million new cases and 1.5 million TB related deaths globally in 2013 [4]. Twenty-two countries account for 80% of the global burden of TB, with nine of these countries located within the South-East Asian and Western Pacific Regions [5]. In Australia the rate of TB notifications has remained relatively stable since 1986. In 2013, there were 1,263 cases reported in Australia, representing a rate of 5.5 per 100 000 [6]. A similar trend has been observed in NSW (Figure 1) with 429 notifications of TB in NSW in 2013, a rate of 5.7 per 100 000 [7].

In 2012 and 2013, nine out of ten notified cases of TB were born overseas (n=819; 90%). There were 76 notifications among Australian born non-Indigenous people and 10 notifications among Aboriginal people. The rate of TB in Aboriginal people in 2012 was seven times higher than the rate for non-Indigenous Australian-born people (4.4 vs 0.6 per 100 000) and over three times higher in 2013 (1.9 vs <0.5 per 100 000) [7]. Accordingly, the most commonly identified risk factors for TB in NSW are being born in a high-risk country and past residence of more than 3 months in a high-risk country. Accordingly, key risk groups include new migrants from endemic countries and healthcare workers returning from working in high risk countries.

Aboriginal people are also a key risk group within Australia [8]. TB control remains a challenge and the disease epidemiology must be considered in a global context, given population movements associated with international travel and migrant populations from high-incidence countries [9].


The most important priorities for TB control and prevention are timely diagnosis and effective treatment [3]. Case management and contact screening undertaken by TB services are important public health measures to minimise transmission and prevent emergence of drug resistance in NSW. This is supported nationally by effective pre [10] and post migration screening undertaken by the Department of Immigration and Border protection in conjunction with jurisdictional TB Prevention and Control Services to minimise the potential for transmission of TB from migrant populations coming to Australia [2].

Figure 1: Number and rate of Tuberculosis notifications in NSW, 1990-2013

The number of patients notified with tuberculosis has remained fairly steady in NSW between 1990 and 2013 with between 400 and 520 notifications per year. Link to data table follows image.
Text alternative


  1. CDC. The Difference between latent TB infection and TB disease factsheet. Centers for Disease Control, Atlanta 21 November 2014. http://www.cdc.gov/tb/publications/factsheets/general/ltbiandactivetb.htm (accessed 28 May 2015).
  2. National Tuberculosis Advisory Committee Multi-drug resistant tuberculosis. Communicable Diseases Intelligence 2007; 31: 406–9.
  3. Tuberculosis control guideline, NSW Health, Sydney (2014) /Infectious/controlguideline/Pages/tuberculosis.aspx (accessed 28 May 2015).
  4. Global tuberculosis report 2014.World Health Organization, Geneva http://www.who.int/tb/publications/global_report/en/ (accessed 25 May 2015).
  5. Global tuberculosis control: WHO report 2011. World Health Organization, Geneva (2011) http://whqlibdoc.who.int/publications/2011/9789241564380_eng.pdf (accessed 28 May 2015)
  6. Toms C, Stapledon R, Waring J, Douglas P, National Tuberculosis Advisory Committee (2015) Tuberculosis notifications in Australia, 2012 and 2013. Submitted to Communicable Diseases Intelligence on 20 February 2015.
  7. NSW Notifiable Conditions Information Management System April 2015 (accessed 30 March 2015).
  8. Lowbridge C, Christensen A, McAnulty J. Tuberculosis in NSW, 2009–2011. NSW Public Health Bulletin,​ https://www.publish.csiro.au/nb/pdf/NBv24n1 (accessed 28 May 2015).
  9. Bareja C, Waring J, Stapledon R, Toms C, Douglas P, National Tuberculosis Advisory Committee (2014) Tuberculosis notifications in Australia, 2011. Communicable Diseases Intelligence; 38(4): E356-E368.
  10. King K, Douglas P, Beath K. Is premigration health screening for tuberculosis worthwhile? Med J Aust 2011; 195 (9): 534-537

The NSW Antenatal Pertussis Vaccination Program

Dr Nathan Saul, Epidemiologist, Communicable Diseases Branch
Sonya Nicholl, Senior Policy Analyst, Immunisation Unit


Pertussis is a bacterial disease which affects the respiratory system. The disease is caused by the organism Bordetella pertussis. It affects individuals of all ages, but is more severe (and can be fatal) in small babies. Despite high vaccination levels, pertussis remains an important disease in NSW, particularly in high risk groups such as infants who are too young to be vaccinated. Epidemics of pertussis occur approximately every three to four years.

Protecting infants at risk of severe disease is a key public health objective. In 2015, the Australian Immunisation Handbook was updated by the National Health and Medical Research Council (NH&MRC) to recommend maternal vaccination during the third trimester of every pregnancy to reduce the burden of disease in young infants.


Beginning in mid-2014 an upward trend in pertussis notifications continued till November 2015 when the outbreak peaked with 2027 cases reported for the month (Figure 1). Following this peak reported cases have declined each month but are still above reported cases pre-outbreak.

School aged children (5 – 9 years and 10 - 14 years) were the most affected age groups, comprising approximately 44 per cent of the notifications in the June 2014 to June 2016 period (Figure 2). High numbers of cases have also been reported in the 0 – 4 years age group - accounting for approximately 16 per cent of notifications in the same period. The peak in reported cases for this age group occurred in February 2016 before beginning to decline. One death was reported in late 2014 which occurred in an unvaccinated infant.

Figure 1. Number of pertussis cases in NSW by month of notification from 1 January 2004 to 30 June 2016

The number of patients notified with pertussis in NSW are less than 500 generally, with epidemics occurring in 2008-9, 2010-11 and 2015-6 seeing peaks to approximately 2000 cases. Link to data table follows image.
Text alternative

Figure 2. Pertussis notifications in NSW by age group June 2014 to June 2016

Between June 2014 and June 2016, the highest number of pertussis notifications in NSW was in the 5 to 9 year age group at approximately 5,000, and lowest in 1 year and less than 1 year old at less than 1000. Link to data table follows image.
Text alternative

Previous NSW infant pertussis prevention strategies

From March 2009, two vaccine-related outbreak control measures were introduced in NSW as part of the response to the increased notifications: a time-limited NSW Health funding of pertussis vaccination for new parents and adult carers of infants less than 12 months old (cocooning strategy); and the first dose of infant pertussis-containing vaccine was promoted to 6 weeks of age from 8 weeks.

From July 2013, NSW Health recommended maternal pertussis vaccine before pregnancy, during pregnancy or immediately post-partum. These recommendations were aligned with the recommendations in The Australian Immunisation Handbook (10th edition) at that time and research completed in NSW which showed that pertussis vaccination of mothers was only effective if given at least 4 weeks before onset of illness in the infant [1]. Free pertussis-containing vaccine was no longer provided for new parents and carers of infants, however NSW Health continued to provide free pertussis vaccine in public hospitals for the opportunistic vaccination of women post-partum who had not received the vaccine in the previous five years.

At the end of 2014, maternal influenza and pertussis immunisation status questions were added to the NSW ObstetriX database to prompt NSW midwives to discuss the need for maternal pertussis vaccination.

Research findings

Research has shown that vaccination during pregnancy is the most effective way to protect infants until they are old enough to be vaccinated. With maternal vaccination, (optimally in the third trimester) infants are protected directly thorough in utero transfer of antibodies and indirectly through reducing the likelihood of the mother acquiring and transmitting pertussis.

Multiple studies have demonstrated the effectiveness of maternal vaccination including an observational study from England which found a 91% reduction in infant pertussis disease through vaccination during the third trimester of pregnancy [3]. A randomised controlled trial published in 2014 also showed that vaccination between 30 – 32 weeks of pregnancy (compared to placebo) was associated with high concentrations of antibodies in infants [4] and likely to provide protection from pertussis in the first 2 months of life. Another study compared the impact on cord antibody levels of vaccination between 27-30 weeks, 31 – 36 weeks and after 36 weeks gestation and found significantly higher antibody levels transferred when the vaccine was given between 27 – 30 weeks [5].

Although inactivated vaccines such as the diphtheria, tetanus and pertussis vaccine (dTpa) are viewed as safe for use during pregnancy by the World Health Organisation (WHO) Global Advisory Committee on Vaccine Safety [7] additional studies directly assessing the safety of pertussis vaccination during pregnancy have been published [4, 8-11]. Evidence (from studies involving more than 40,000 participants) suggests that vaccination during pregnancy is safe for both the mother and baby. Studies, including a large observational study and a randomised clinical trial, have found no increased risk of adverse events or adverse pregnancy outcomes such as stillbirth, hypertensive disorder of pregnancy, preterm birth or small for gestational age birth [8-11].

Cost analysis from the US found that pertussis vaccination during pregnancy would avert more infant cases and deaths at a lower cost than vaccination after birth even when combined with cocooning strategies [6].

To inform health care workers and the community NSW health prepared an evidence review on the effectiveness, safety, and timing of maternal pertussis vaccination.

NSW Antenatal Pertussis Vaccination Program

The NSW Antenatal Pertussis Vaccination Program commenced on 1 April 2015 offering free diphtheria, tetanus and pertussis (dTpa) vaccine to all pregnant women in the third trimester (preferably at 28 weeks). Boostrix® vaccine is provided free to GPs, Aboriginal Medical Services and antenatal clinics for all pregnant women in the third trimester and over 165 000 doses of vaccine have been distributed since the commencement of the program up to 31 May 2016.

Complete maternal vaccine coverage data is not readily available, however in 2016, the ObstetriX database will transition to eMaternity. This transition will facilitate consistent statewide reporting on maternal vaccinations.

A Health Education and Training Institute (HETI) education module for midwives has been developed for staff employed in public facilities and plans are progressing to make the module available to staff in private facilities.

A website (health.nsw.gov.au/protectnewborns) provides detailed program information including brochures (translated into 23 community languages), Aboriginal specific resources, evidence review, frequently asked questions and guidelines. Communication packages were also distributed to immunisation providers at the commencement of the program.

18-month Diphtheria Tetanus and Pertussis (DTPa) dose

In 2003 the 18-month pertussis booster dose was removed from the National Immunisation Program (NIP). This may have contributed to increased disease rates subsequently observed in young children by prolonging the time interval between the completion of the primary course at six month of age and the next booster at four years of age, in association with a change in vaccine type with decreased efficacy and longevity [13].

In 2013 the NH&MRC recommended that an additional booster dose of a pertussis-containing vaccine in the second year of life would minimise the likelihood of the child developing pertussis prior to their scheduled booster dose at 4 years due to waning immunity [13].

An 18-month booster has been funded by the Australian Government and has been included on the NIP for all children born from 1 October 2014 with the new program commencing in March 2016.

Useful resources and websites


  1. Quinn HE, Snelling TL, Habig A, Chiu C, Spokes PJ, McIntyre PB. Parental Tdap Boosters and Infant Pertussis: A Case-Control Study. Pediatrics 2014;134(4):713–720.
  2. Spokes, P.J., Quinn, H.E. and McAnulty, J.M. Review of the 2008-2009 pertussis epidemic in NSW: notifications and hospitalisations. NSW Public Health Bulletin, 2010. 21(7-8):167-173.
  3. Amirthalingam, G., et al., Effectiveness of maternal pertussis vaccination in England: an observational study. The Lancet 2015. 384 1521-1528.
  4. Munoz, F.M., et al., Safety and Immunogenicity of Tetanus Diphtheria and Acellular Pertussis (Tdap) Immunization During Pregnancy in Mothers and Infants. Journal of the American Medical Association 2014. 311 no.17 (1760-1769.
  5. Raya, B.A. et al., The effect of timing of maternal tetanus, diphtheria, and acellular pertussis (Tdap) immunization during pregnancy on newborn pertussis antibody levels – a prospective study. Vaccine, 2014. 32: 5787-5793
  6. Terranella, A. et al., Pregnancy Dose Tdap and Postpartum Cocooning to Prevent Infant Pertussis: A Decision Analysis. Obstetrical & Gynecological Survey 2013.68(9): p.615-616
  7. WHO, Global Advisory Committee on Vaccine Safety, 12-13 June 2013. WHO Weekly Epidemiological Record 2013. 88: p. 301-12.
  8. Donegan, K., King, B. and Bryan, P. Safety of pertussis vaccination in pregnant women in UK: observational study. British Medical Journal 2014.349:g4219.doi: 10.1136/bmj.g4219 (Published 11 July 2014)
  9. Kharbanda, E.O et al., Evaluation of the association of maternal pertussis vaccination with obstetric events and birth outcomes. JAMA, 2014. 312(18): p. 1897-1904.
  10. Shakib, J.H. et al Tetanus, Diphtheria, Acellular Pertussis Vaccine during Pregnancy: Pregnancy and Infant Health Outcomes. The Journal of Pediatrics 2011. 163(5): p. 1422-1426.e4.
  11. Zheteyeva, Y.A. et al., Adverse event reports after tetanus toxoid,reduced diphtheria toxoid, and acellular pertussis vaccines in pregnant women. American Journal of Obstetrics and Gynecology 2012. 207(1): p. 59.e1-59.e7.
  12. National Health and Medical Research Council (NH&MRC) 2013, The Australian Immunisation Handbook (10th edition), Commonwealth of Australia, Canberra
  13. Pillsbury, A., Quinn, H.E. and McIntyre, P. Australian Vaccine Preventable Disease Epidemiological Review Series: Pertussis, 2006-2012. Communicable Disease Intelligence 2014. 38 no3 pE179-E104

Current as at: Wednesday 24 March 2021
Contact page owner: Health Protection NSW