The Australasian Society for Infectious Diseases and Refugee Health Network of Australia recommendations for health assessment for people from refugee-like backgrounds: an abridged outline

There are currently more than 65 million people who have been forcibly displaced worldwide, including 21.3 million people with formal refugee status, over half of whom are aged under 18 years.1 More than 15 000 refugees have resettled in Australia in the 2015–16 financial year, which includes a proportion of the 12 000 refugees from Syria and Iraq recently added to Australia’s humanitarian intake.2 In addition, around 30 000 asylum seekers who arrived by plane or boat are currently in Australia awaiting visa outcomes.3

People from refugee-like backgrounds are likely to have experienced disruption of basic services, poverty, food insecurity, poor living conditions and prolonged uncertainty; they may have experienced significant human rights violations, trauma or torture. These circumstances place them at increased risk of complex physical and mental health conditions. They face numerous barriers to accessing health care after arrival in Australia, such as language, financial stress, competing priorities in the settlement period, and difficulties understanding and navigating the health care system.4–6 Most people require the assistance of an interpreter for clinical consultations.7 Offering a full health assessment to newly arrived refugees and asylum seekers is a positive step towards healthy settlement, and helps manage health inequity through the provision of catch-up immunisation and the identification and management of infectious and other health conditions.

These guidelines update the Australasian Society of Infectious Diseases (ASID) guidelines for the diagnosis, management and prevention of infectious diseases in recently arrived refugees8 published in 2009 and previously summarised in the MJA.9 When these recommendations were first published, more than 60% of humanitarian entrants arriving in Australia were from sub-Saharan Africa10 and had a high prevalence of malaria, schistosomiasis and hepatitis B virus (HBV) infection.11–15 The initial guidelines were primarily intended to help specialists and general practitioners to diagnose, manage and prevent infectious diseases. Since then, there have been changes in refugee-source countries — with more arrivals from the Middle East and Asia and fewer from sub-Saharan Africa16,17 — and an increased number of asylum seekers arriving by boat,18 alongside complex and changing asylum seeker policies and changes in health service provision for these populations. In this context, we reviewed the 2009 recommendations to ensure relevance for a broad range of health professionals and to include advice on equitable access to health care, regardless of Medicare or visa status. The revised guidelines are intended for health care providers caring for people from refugee-like backgrounds, including GPs, refugee health nurses, refugee health specialists, infectious diseases physicians and other medical specialists.

This article summarises the full guidelines, which contain detailed literature reviews, recommendations on diagnosis and management along with explanations, supporting evidence and links to other resources. The full version is available at http://www.asid.net.au/documents/item/1225.

Methods

The guideline development process is summarised in Box 1. The two key organisations developing these guidelines are ASID and the Refugee Health Network of Australia. ASID is Australia’s peak body representing infectious diseases physicians, medical microbiologists and other experts in the fields of the prevention, diagnosis and treatment of human and animal infections. The Refugee Health Network is a multidisciplinary network of health professionals across Australia with expertise in refugee health.20

We defined clinical questions using the PIPOH framework (population, intervention, professionals, outcomes and health care setting).21 The chapter authors and the Expert Advisory Group developed recommendations based on reviews of available evidence, using systematic reviews where possible. Australian prevalence data also informed screening recommendations; for example, the low reported prevalence of chlamydia (0.8–2.0%) infections and absence of gonorrhoea infections in refugee cohorts in Australia13,22–24 (and in other developed countries25–27) informed the new recommendation for risk-based sexually transmitted infection (STI) screening.

Despite the intention to assign levels of evidence to each recommendation, there was limited published high level evidence in most areas, and virtually all recommendations are based on expert consensus. Consensus was not reached regarding the recommendations relating to human immunodeficiency virus (HIV) and STIs.

The term “refugee-like” is used to describe people who are refugees under the United Nations Refugee Convention,28 those who hold a humanitarian visa, people from refugee-like backgrounds who have entered under other migration streams, and people seeking asylum in Australia. “Refugee-like” acknowledges that people may have had refugee experience in their countries of origin or transit, but do not have formal refugee status.

Current pre-departure screening

All permanent migrants to Australia have a pre-migration immigration medical examination 3–12 months before departure,29 which includes a full medical history and examination. Investigations depend on age, risk factors and visa type,30 and include:

a chest x-ray for current or previous tuberculosis ([TB]; age ≥ 11 years);
screening for latent TB infection with an interferon-γ release assay or tuberculin skin test (for children aged 2–10 years, if they hold humanitarian visas, come from high prevalence countries or have had prior household contact);
HIV serology (age ≥ 15 years, unaccompanied minors);
hepatitis B surface antigen (HBsAg) testing (pregnant women, unaccompanied minors, onshore protection visas, health care workers);
hepatitis C virus (HCV) antibody testing (onshore protection visas, health care workers); and
syphilis serology (age ≥ 15 years, humanitarian visas, onshore protection visas).

Humanitarian entrants are also offered a voluntary pre-departure health check depending on departure location and visa subtype.31 The pre-departure health check includes a rapid diagnostic test and treatment for malaria in endemic areas; empirical treatment for helminth infections with a single dose of albendazole; measles, mumps and rubella vaccination; and yellow fever and polio vaccination where relevant. The current cohort of refugees arriving from Syria will have extended screening incorporating the immigration medical examination and pre-departure health check, with additional mental health review and immunisations.

People seeking asylum who arrived by boat have generally had a health assessment on arrival in immigration detention — although clinical experience suggests that investigations and detention health care varies, especially for children. However, asylum seekers who arrived by plane will not have had a pre-departure immigration medical examination.

General recommendations

Our overarching recommendation is to offer all people from refugee-like backgrounds, including children, a comprehensive health assessment and management plan, ideally within 1 month of arrival in Australia. This assessment can be offered at any time after arrival if the initial contact with a GP or clinic is delayed, and should also be offered to asylum seekers after release from detention. Humanitarian entrants who have been in Australia for less than 12 months are eligible for a GP Medicare-rebatable health assessment. Such assessments may take place in a primary care setting or in a multidisciplinary refugee health clinic. Documented overseas screening and immunisations, and clinical assessment should also guide diagnostic testing.

Health care providers should adhere to the principles of person-centred care when completing post-arrival assessments.32,33 These include: respect for the patient’s values, preferences and needs; coordination and integration of care with the patient’s family and other health care providers; optimising communication and education, provision of interpreters where required (the Doctors Priority Line for the federal government-funded Translating and Interpreting Service is 1300 131 450) and use of visual and written aids and teach-back techniques to support health literacy.34 It is important to explain that a health assessment is voluntary and results will not affect visa status or asylum claims.

Specific recommendations

Recommendations are divided into two sections: infectious and non-infectious conditions. Box 2 provides a checklist of all recommended tests, and Box 3 sets out details of country-specific recommendations. A brief overview is provided below. For more detailed recommendations regarding management, follow-up and considerations for children and in pregnancy, see the full guidelines.

Infectious conditions

TB:

Offer latent TB infection testing with the intention to offer preventive treatment and follow-up.
Offer screening for latent TB infection to all people aged ≤ 35 years.
Children aged 2–10 years may have been screened for latent TB infection as part of their pre-departure screening.
Screening and preventive treatment for latent TB infection in people > 35 years will depend on individual risk factors and jurisdictional requirements in the particular state or territory.
Use either a tuberculin skin test or interferon-γ release assay (blood) to screen for latent TB infection.
A tuberculin skin test is preferred over interferon-γ release assay for children < 5 years of age.
Refer patients with positive tuberculin skin test or interferon-γ release assay results to specialist tuberculosis services for assessment and exclusion of active TB and consideration of treatment for latent TB infection.
Refer any individuals with suspected active TB to specialist services, regardless of screening test results.

Malaria:

Investigations for malaria should be performed for anyone who has travelled from or through an endemic malaria area (Box 3), within 3 months of arrival if asymptomatic, or any time in the first 12 months if there is fever (regardless of pre-departure malaria testing or treatment).
Test with both thick and thin blood films and an antigen-based rapid diagnostic test.
All people with malaria should be treated by, or in consultation with, a specialist infectious diseases service.

HIV:

Offer HIV testing to all people aged ≥ 15 years and all unaccompanied or separated minors, as prior negative tests do not exclude the possibility of subsequent acquisition of HIV (note that consensus was not reached regarding this recommendation).

HBV:

Offer testing for HBV infection to all, unless it has been completed as part of the immigration medical examination.
A complete HBV assessment includes HBsAg, HB surface antibody and HB core antibody testing.
If the HBsAg test result is positive, further assessment and follow-up with clinical assessment, abdominal ultrasound and blood tests are required.

HCV:

Offer testing for HCV to people if they have:
- risk factors for HCV;
- lived in a country with a high prevalence (> 3%) of HCV (Box 3); or
- an uncertain history of travel or risk factors.
Initial testing is with an HCV antibody test. If the result is positive, request an HCV RNA test.
If the HCV RNA test result is positive, refer to a doctor accredited to treat HCV for further assessment.

Schistosomiasis:

Offer blood testing for Schistosoma serology if people have lived in or travelled through endemic countries (Box 3).
If serology is negative, no follow-up is required.
If serology is positive or equivocal:
- treat with praziquantel in two doses of 20 mg/kg, 4 hours apart, orally; and
- perform stool microscopy for ova, urine dipstick for haematuria, and end-urine microscopy for ova if there is haematuria.
If ova are seen in urine or stool, evaluate further for end-organ disease.

Strongyloidiasis:

Offer blood testing for Strongyloides stercoralis serology to all.
If serology is positive or equivocal:
- check for eosinophilia and perform stool microscopy for ova, cysts and parasites; and
- treat with ivermectin 200 μg/kg (weight ≥ 15 kg), on days 1 and 14 and repeat eosinophil count and stool sample if abnormal.
Refer pregnant women or children < 15 kg for specialist management.

Intestinal parasites:

Check full blood examination for eosinophilia.
If pre-departure albendazole therapy is documented:
- if there are no eosinophilia and no symptoms, no investigation or treatment is required; and
- if there is eosinophilia, perform stool microscopy for ova, cysts and parasites, followed by directed treatment.
If no documented pre-departure albendazole therapy, depending on local resources and practices, there are two acceptable options:
- empirical single dose albendazole therapy (age > 6 months, weight < 10 kg, dose 200 mg; weight ≥ 10 kg, dose 400 mg; avoid in pregnancy, class D drug); or
- perform stool microscopy for ova, cysts and parasites, followed by directed treatment.

Helicobacter pylori:

Routine screening for H. pylori infection is not recommended.
Screen with either stool antigen or breath test in adults from high risk groups (family history of gastric cancer, symptoms and signs of peptic ulcer disease, or dyspepsia).
Children with chronic abdominal pain or anorexia should have other common causes of their symptoms considered in addition to H. pylori infection.
Treat all those with a positive test (see the full guidelines for details, tables 1.5 and 9.1).

STIs:

Offer an STI screen to people with a risk factor for acquiring an STI or on request. Universal post-arrival screening for STIs for people from refugee-like backgrounds is not supported by current evidence.
A complete STI screen includes a self-collected vaginal swab or first pass urine nucleic acid amplification test and consideration of throat and rectal swabs for chlamydia and gonorrhoea, and serology for syphilis, HIV and HBV.
Syphilis serology should be offered to unaccompanied and separated children < 15 years.

Skin conditions:

The skin should be examined as part of the initial physical examination.
Differential diagnoses will depend on the area of origin (see table 11.1 in full guidelines for details).

Immunisation:

Provide catch-up immunisation so that people of refugee background are immunised equivalent to an Australian-born person of the same age.
In the absence of written immunisation documentation, full catch-up immunisation is recommended.
Varicella serology is recommended for people aged ≥ 14 years if there is no history of natural infection.
Rubella serology should be completed in women of childbearing age.

Non-infectious conditions

Anaemia and other nutritional problems:

Offer full blood examination screening for anaemia and other blood conditions to all.
Offer screening for iron deficiency with serum ferritin to children, women of childbearing age, and men who have risk factors.
Check vitamin D status as part of initial health screening in people with one or more risk factors for low vitamin D.
People with low vitamin D should be treated to restore their levels to the normal range with either daily dosing or high dose therapy, paired with advice about sun exposure.
Consider screening for vitamin B₁₂ deficiency in people with history of restricted food access, especially those from Bhutan, Afghanistan, Iran and the Horn of Africa.

Chronic non-communicable diseases in adults:

Offer screening for non-communicable diseases in line with the Royal Australian College of General Practitioners Red Book35 recommendations, including assessment for:
- smoking, nutrition, alcohol and physical activity;
- obesity, diabetes, hypertension, cardiovascular disease, chronic obstructive pulmonary disease and lipid disorders; and
- breast, bowel and cervical cancer.
Assess diabetes and cardiovascular disease risk earlier for those from regions with a higher prevalence of non-communicable diseases, or those with an increased body mass index or waist circumference.

Mental health:

A trauma informed assessment of emotional wellbeing and mental health is part of post-arrival screening. Being aware of the potential for past trauma and impact on wellbeing is essential, although it is generally not advisable to ask specifically about details in the first visits.
Consider functional impairment, behavioural difficulties and developmental progress as well as mental health symptoms when assessing children.

Hearing, vision and oral health:

A clinical assessment of hearing, visual acuity and dental health should be part of primary care health screening.

Women’s health:

Offer women standard preventive screening, taking into account individual risk factors for chronic diseases and bowel, breast and cervical cancer.
Consider pregnancy and breastfeeding and offer appropriate life stage advice and education, such as contraceptive advice where needed, to all women, including adolescents.
Practitioners should be aware of clinical problems, terminology and legislation related to female genital mutilation or cutting and forced marriage.

Box 1 –
Guideline development process

An EAG, consisting of refugee health professionals, was formed and it included two ID physicians, an ID and general physician, two GPs, a public health physician, a general paediatrician and a refugee health nurse. An editorial subgroup was also formed.
The EAG determined the list of priority conditions in consultation with refugee health specialists and RACGP Refugee Health Special Interest Group clinicians, incorporating information from consultations with refugee background communities19 and previous ASID refugee health guidelines.
Each condition was assigned to a primary specialist author with paediatrician and primary care or specialist co-authors. Twenty-eight authors from six states and territories were involved in writing the first draft.
The EAG reviewed the first draft to ensure consistency with the framework and the rest of the guidelines. They were then revised by the primary authors.
External expert review authors reviewed the second draft and they were then revised by the primary authors.
The EAG and the refugee health nurse subcommittee reviewed the third draft.
The stakeholders reviewed the fourth draft: ASID, NTAC, RHeaNA, RACGP Refugee Health Special Interest Group, RACP, RACP AChSHM, the Victorian Foundation for the Survivors of Torture, the Multicultural Centre for Women’s Health, the Asylum Seeker Resource Centre, the Ethnic Communities Council of Victoria and community members.
The comments from the stakeholders were returned to the authors for review and the EAG compiled the final version.
ASID, RACP, NTAC and AChSHM endorsed the final version.

AChSHM = Australasian Chapter of Sexual Health Medicine. ASID = Australasian Society for Infectious Diseases. EAG = Expert Advisory Group. GP = general practitioner. ID = infectious diseases. NTAC = National Tuberculosis Advisory Council. RACGP = Royal Australian College of General Practitioners. RACP = Royal Australasian College of Physicians. RHeaNA = Refugee Health Network of Australia. Adapted from the ASID and RHeaNA Recommendations for comprehensive post-arrival health assessment for people from refugee-like backgrounds (2016; https://www.asid.net.au/documents/item/1225) with permission from ASID.

Box 2 –
Short checklist of recommendations for post-arrival health assessment of people from refugee-like backgrounds

Offer test to

Test

Comments and target condition

All

Full blood examination

Anaemia, iron deficiency, eosinophilia

Hepatitis B serology (HBsAg, HBsAb, HBcAb)

HBsAg testing introduced overseas in 2016 for Syrian and Iraqi refugee cohort and may have been completed in other groups

Strongyloides stercoralis serology

Strongyloidiasis

HIV serology*

≥ 15 years or unaccompanied or separated minor
Also part of IME for age ≥ 15 years

TST or IGRA

Offer test if intention to treat. All ≤ 35years; if≥ 35 years, depends on risk factors and local jurisdiction. TST preferred for children < 5 yearsTST or IGRA testing introduced in 2016 as part of IME for children 2–10 years (humanitarian entrants, high prevalence countries, prior household contact)
LTBI

Varicella serology

≥ 14 years if no known history of disease
Determine immunisation status

Visual acuity

Vision status, other eye disease

Glaucoma assessment

Africans > 40 years and others > 50 years

Dental review

Caries, periodontal disease, other oral health issues

Hearing review

Hearing impairment

Social and emotional wellbeing and mental health

Mental illness, trauma exposure, protective factors

Developmental delay or learning concerns

Children and adolescents
Developmental issues, disability, trauma exposure

Preventive health as per RACGP35

Non-communicable diseases, consider screening earlier than usual age

Catch-up vaccinations

Vaccine preventable diseases, including hepatitis B

Risk-based

Rubella IgG

Women of childbearing age
Determines immunisation status

Ferritin

Men who have risk factors, women and childrenIron deficiency anaemia

Vitamin D, also check calcium, phosphate, and alkaline phosphatase in children

Risk factors if dark skin or lack of sun exposure
Low vitamin D, rickets

Vitamin B₁₂

Arrival < 6 months, food insecurity, vegan diet or from Bhutan, Afghanistan, Iran or Horn of Africa
Nutritional deficiency, risk for developmental disability in infants

First pass urine or self-obtained vaginal swabs for gonorrhoea and chlamydia PCR

Risk factors for STI or on request*

Syphilis serology

Risk factors for STIs, unaccompanied or separated minors. Part of IME in humanitarian entrants aged ≥ 15 years

Helicobacter pylori stool antigen or breath test

Gastritis, peptic ulcer disease, family history of gastric cancer, dyspepsia

Stool microscopy (ova, cysts and parasites)

If no documented pre-departure albendazole or persisting eosinophilia despite albendazoleIntestinal parasites

Country-based (Box 3)

Schistosoma serology

Schistosomiasis

Malaria thick and thin films and rapid diagnostic test

Malaria

HCV Ab, and HCV RNA if HCV Ab positive

HCV, also test if risk factors, regardless of country of origin

HBcAb = hepatitis B core antibody. HBsAb = hepatitis B surface antibody. HBsAg = hepatitis B surface antigen. HCV = hepatitis C virus. HCV Ab = hepatitis C antibody. HIV = human immunodeficiency virus. IGRA = interferon-γ release assay. IME = immigration medical examination. LBTI = latent tuberculosis infection. PCR = polymerase chain reaction. TST = tuberculin skin test. * The panel did not reach consensus on these recommendations. See full guideline at http://www.asid.net.au/documents/item/1225 for details.

Box 3 –
Top 20 countries of origin for refugees and asylum seekers2,3,16 and country-specific recommendations for malaria, schistosomiasis and hepatitis C screening*

Country of birth

Malaria36

Schistosomiasis37

Hepatitis C^†38

Afghanistan

Bangladesh

Yes

Bhutan

Yes

Burma

Yes

China

Congo

Yes

Egypt

Yes

Eritrea

Yes

India

Yes

Iran

Iraq

Yes

Lebanon

Pakistan

Yes

Somalia

Yes

Sri Lanka

Yes

Stateless^‡

Yes

Sudan

Yes

Syria

Yes

Consider

Vietnam

* There are regional variations in the prevalence of these conditions within some countries. We have taken the conservative approach of recommending screening for all people from an endemic country rather than basing the recommendation on exact place of residence. Note that some refugees and asylum seekers may have been exposed during transit through countries not listed here. See full guideline for further details. † People with risk factors for hepatitis C should be tested regardless of country of origin. ‡ “Stateless” in this table refers to people of Rohingyan origin. Adapted from the ASID and RHeaNA Recommendations for comprehensive post-arrival health assessment for people from refugee-like backgrounds (2016; https://www.asid.net.au/documents/item/1225) with permission from ASID.

The microbiology of crocodile attacks in Far North Queensland: implications for empirical antimicrobial therapy

Wound infections are common after crocodile attacks and, therefore, prophylactic antimicrobial therapy is advised. However, there are limited data to guide recommendations for the optimal empirical regimen.

In a study from 1992,1 six of 11 survivors of crocodile attacks from Australia’s Northern Territory developed wound infection. The organisms isolated included Aeromonas hydrophila and Enterococcus species, Clostridium species, Pseudomonas aeruginosa and Proteus species, Staphylococcus epidermidis and Burkholderia pseudomallei. As a result, the authors advocated an empirical antibiotic regimen of ceftazidime, penicillin and metronidazole, with the addition of flucloxacillin to treat the patient’s skin flora.1 The Australian Therapeutic Guidelines do not discuss crocodile attacks specifically, but suggest giving oral amoxycillin–clavulanate to people with animal bite wounds at high risk of developing infection, and to patients with established mild infection. For more severe infections, intravenous piperacillin–tazobactam is recommended.2

To validate these recommendations, we reviewed the medical records of 14 of the 15 patients attacked by crocodiles who presented to Cairns Hospital in Queensland, Australia, after 1990 (one chart had been destroyed). Patients were aged 8–70 years and 13 were males. Wild saltwater crocodiles were responsible for seven attacks, farmed saltwater crocodiles for five and wild freshwater crocodiles for two. At presentation, nine patients had wound swabs collected; skin and soft tissue infection was already clinically apparent in four people. Organisms were isolated in six patients where swabs were collected (Box). Eleven of the 14 patients had surgery, with three requiring repeat debridement. Three further patients underwent delayed primary closure and two others required joint washouts. All patients received empirical antibiotics, but the selected agents varied enormously: ceftriaxone was the most commonly prescribed, but metronidazole, gentamicin, doxycycline, cephazolin, flucloxacillin and penicillin were also administered. No patients developed metastatic infection and all survived, although two of them lost digits.

Our findings highlight the diversity of organisms isolated from wounds caused by crocodile attacks. These bacteria can originate from the crocodile’s oral flora, the patient’s skin or can be acquired from the water or soil during the attack. The oral and cloacal flora of Australian crocodiles contain a myriad of organisms, including Aeromonas hydrophila, Pseudomonas aeruginosa, and Proteus and Salmonella species.3 While Aeromonas hydrophila — an organism found in fresh and brackish water — was notably absent in our study, it was the most common isolate in the NT series.1

The excellent outcomes seen in this study are probably primarily explained by prompt, effective surgical care,4,5 but antibiotics may have prevented infective complications. Although the regimen recommended in the NT series would have covered most of the Queensland isolates, it is relatively complex. Based on the isolates in the two series, an empirical regimen of oral amoxycillin–clavulanate for high risk wounds and mild infections would appear appropriate, reserving intravenous piperacillin–tazobactam for more severe infections. These treatments accord with the recommendations of the Australian Therapeutic Guidelines. It is essential to collect tissue cultures to facilitate de-escalation or modification of therapy if rare or resistant organisms, such as Burkholderia pseudomallei or Vibrio species, are isolated. In addition, tetanus should also be considered, with immunisation where appropriate.

Box –
Injuries sustained, surgical intervention and organisms isolated in survivors of crocodile attacks

Patient

Crocodile

Injury sustained

Infection evident

Surgical intervention

Time to debridement (hours)

Empirical antibiotics

Organisms isolated from wound swab

Age (years)

Sex

Male

Farmed saltwater

Superficial skin and soft tissue wound of lower limb

Yes

No surgical intervention

N/A

Benzylpenicillin, flucloxacillin, gentamicin

Proteus vulgarisCitrobacter (diversus) koseriGroup G Streptococcus

Female

Wild saltwater

Superficial skin and soft tissue wound of torso

Debridement and washout, delayed primary closure

Ceftriaxone

Candida albicans*

Female

Wild saltwater

Fracture, deep skin and soft tissue wound of upper limb and face

Debridement and washout, internal fixation, skin graft

Ceftriaxone, metronidazole, gentamicin

Bacillus cereus*

Male

Wild saltwater

Crush injury and fractures of upper and lower limbs

Yes

Debridement and washout, tibial nail, joint washout

Ceftriaxone, metronidazole, gentamicin

Bacillus cereus*

Male

Farmed saltwater

Superficial skin and soft tissue wound of upper limb

No surgical intervention

N/A

Ceftriaxone, metronidazole

Staphylococcus aureus

Male

Wild saltwater

Fractures of upper and lower limbs

Yes

Multiple debridements and washouts, joint washouts, knee reconstruction

Cephazolin, metronidazole, doxycycline

Pseudomonas aeruginosaEnterococcus spp.

N/A = not applicable. * Likely represents colonisation rather than true infection.

Treatment of latent tuberculosis infections in the Darwin region

As it is estimated that one-third of the world population have a latent tuberculosis infection (LTBI), treatment to prevent active tuberculosis is an essential component of the World Health Organization “End TB Strategy”.1

To inform and evaluate practice, we undertook a cohort study of people in the Darwin region (estimated population, 140 000; 25% Indigenous Australians, 25% overseas-born residents) diagnosed with LTBI according to Northern Territory guidelines2 during June 2013 – July 2014. Diagnosis was based on a positive Mantoux test result2 and the absence of radiological and clinical evidence for active tuberculosis. Demographic and treatment acceptance and compliance data were collected from the sole treatment centre serving the region. The recommended therapy was 9 months’ treatment with isoniazid, or 4 months’ treatment with rifampicin if isoniazid was contraindicated.2 Treatment adherence was assessed monthly on the basis of clinic attendance, self-reported adherence, and collection of the medication.

During the study period, 573 people were diagnosed with LTBI, of whom 422 (74%) were overseas-born, 81 (14%) were Indigenous Australians, and 70 (12%) were non-Indigenous Australians. The age range was 0–77 years (median, 32 years); 61% were male. The proportions of people diagnosed with LTBI who were offered, accepted and completed treatment are shown in the Box. Uncertainty on the part of the physician about an individual’s ability to complete treatment was the most common reason for not offering treatment, including to members of transient populations, such as those with short prison sentences and immigration detainees. Most patients who did not complete therapy had been lost to follow-up, either moving interstate (31%) or defaulting without a reason being recorded (25%). Outcome data for people moving interstate were not collected, as there are no mechanisms for routinely sharing such data between Australian states, and forwarding addresses were unavailable. The 55% completion rate therefore probably underestimates the proportion of those who completed treatment.

Parents and guardians of all 28 children under 6 years of age accepted treatment for their children, 12 of whom (43%) completed treatment, including six of 11 who were contacts of people with active tuberculosis, four of 16 immigration detainees, and three of seven refugees. Five children did not, however, commence treatment (three immigration detainees, two refugees), and 11 moved interstate without completing treatment. Nine of those moving interstate were immigration detainees, highlighting the transiency of this population and the uncertainty of outcomes arising from a lack of feedback between states about LTBI treatment compliance.

Indigenous Australians were significantly more likely to accept treatment than overseas-born people (odds ratio [OR], 4.46; 95% CI, 1.55–12.8) or non-Indigenous Australians (OR, 7.69; 95% CI, 2.33–25.4). Overseas-born patients were less likely to complete treatment than Indigenous (OR, 1.34; 95% CI, 0.66–2.72) or non-Indigenous Australians (OR, 1.38; 95% CI, 0.56–3.41). This finding, however, was not statistically significant, and potentially confounded by the fact that all 36 patients who moved interstate were overseas-born, so that completion for this population was possibly higher.

Similar to the findings of other Australian studies, 45% of patients who accepted treatment did not complete it, representing missed opportunities for preventing disease.3,4 Uncertainty about treatment adherence by overseas-born people moving interstate indicates that national data sharing and collaboration between tuberculosis services should be improved. LTBI treatment could then be evaluated according to WHO recommendations, and targeted measures to improve treatment outcomes for this high-risk population implemented.1,3 Further, the reasons for not completing treatment were often unknown; communicating with non-adherent patients would identify problems and enable targeted interventions for improving compliance.

Encouragingly, we found high uptake of treatment by Indigenous Australians, which may help reduce the disproportionately high incidence of active tuberculosis in this population, compared with non-Indigenous Australians.

Box –
The proportions of people diagnosed with latent tuberculosis infection who were offered, accepted and completed treatment, Darwin, June 2013 – July 2014

	Total	Age group (years)
	Total	0–5	6–15	16–35	> 35

People diagnosed with a latent tuberculosis infection (LTBI)	573	32	56	244	241
Reasons for LTBI screening: asylum seeker/refugee (24%); health care worker (19%); tuberculosis contact (17%); (pre-)immunosuppression (7%); school student (overseas-born) (6%); medical referral (6%); incarcerated (6%); immigration health undertaking (3%); defence force personnel (3%); other (9%)
Offered treatment	374 of 573 (65%)	28 (88%)	48 (86%)	153 (63%)	145 (60%)
Reasons for not offering treatment: short term detention/prison sentence (physician uncertain about future adherence) (37%); low risk (35%); excessive alcohol use or liver disease (6%); prior LTBI treatment (4%); pregnant/lactation (4%); depression (2%); other (14%)
Accepted treatment	265 of 374 (71%)	28 (100%)	38 (79%)	103 (67%)	96 (66%)
Completed treatment	147 of 265 (55%)	12 (43%)	26 (68%)	56 (54%)	53 (55%)
Reasons for incomplete treatment: moved away from treatment centre (31%); no reason given/defaulted (25%); did not commence treatment (20%); elevated liver enzyme levels (5%); peripheral neuropathy (3%); patient died of disease other than tuberculosis (3%); rash (2%); other (12%)

Trends in the prevalence of hepatitis B infection among women giving birth in New South Wales

The known In NSW, HBV vaccination of infants born to women at high risk commenced in 1987, and catch-up vaccination programs for adolescents in 1999.

The new Among women giving birth, targeted infant and school-based adolescent vaccination programs were associated with an 80% decline in HBV prevalence among Indigenous women by 2012. HBV prevalence in Indigenous women was higher in rural and remote NSW than in major cities, but among non-Indigenous and overseas-born women it was higher in cities.

The implications HBV prevention programs for Indigenous Australians should focus on regional and remote NSW and those for migrant populations on major cities. Antenatal HBV screening can be used to monitor population HBV prevalence and the impact of vaccination programs.

Chronic infection with the hepatitis B virus (HBV) can cause serious liver disease, and contributes worldwide to a significant burden of disease. Most chronic infections are acquired early in life, predominantly by maternal transmission.1 While its prevalence in Australia is generally considered to be low (under 2%), the prevalence of HBV infections in Aboriginal and Torres Strait Islander (hereafter: Indigenous)2 people and in some migrant populations3 has been substantial.

A three-dose vaccine that is 95% effective in preventing HBV infection4 has been available in Australia since the early 1980s.5 In New South Wales, a targeted HBV vaccination program commenced in 1987.6 The program offered vaccination for babies born to parents from population groups considered to be at higher risk of HBV infection (defined as HBV prevalence ≥ 5%), including Indigenous Australians.7 In 1997, the National Health and Medical Research Council recommended universal HBV catch-up vaccination of children aged 10–16 years;8 in NSW, this was provided from 1999 to adolescents born since 1983 by general practitioners.9 The National Immunisation Program Schedule included universal infant HBV vaccination from May 2000. During 2004–2013, this was complemented by a NSW-wide school-based HBV vaccination catch-up program for year 7 students (born since 1991; online Appendix 1).5,7 In NSW, coverage through the universal infant program was reported to have exceeded 95% since 2003,10 and about 60% of eligible children not vaccinated as infants had been vaccinated through the school-based catch-up program in 2011 and 2012.11

To assess the impact of the vaccination programs on HBV prevalence in NSW, we determined its prevalence in women giving birth, as in Australia they are routinely screened for HBV during pregnancy.12 Our methodology was similar to that used in earlier studies that linked records of women giving birth and HBV infection notifications.2,3

Methods

Data sources and linkage

Data from two statutory registers were linked. The NSW Perinatal Data Collection (PDC) records all births in NSW of babies of at least 400 grams birth weight or 20 weeks’ gestation. The PDC contains details about the mother, such as year and country of birth, parity, postcode of residence, and Indigenous status, and about the birth, including the date of delivery and outcome. The NSW Notifiable Conditions Information Management System (NCIMS) is a population-based surveillance system that records reports of conditions deemed notifiable under the NSW Public Health Acts 1991 and 2010.13,14 The Act requires notification to NCIMS by any laboratory detecting HBV surface antigen (HBsAg), a marker of HBV infection, in a specimen submitted for diagnostic testing. The NCIMS records personal details, including date of birth, sex, postcode, and classification of the report as newly acquired hepatitis B infection or infection of unspecified duration (based on standard definitions15), notification date, and either the estimated onset date or date of the diagnostic test.

PDC records of women giving birth between January 1994 and December 2012 and NCIMS HBV notifications for the same period were available. Records from the two registers were linked by probabilistic matching of personal identifying details; this was conducted by the NSW Centre for Health Record Linkage (CHeReL), independently of the study investigators, to whom de-identified, linked data were provided for analysis. The reported false positive and negative rates for CHeReL linkage are about 0.5%.16

Study population and definitions

After linkage, we restricted our study population to women resident in NSW — using their postcode on the PDC record — of reproductive age (10–55 years at time of giving birth) who gave birth to their first child (ie, parity null) between January 2000 (when routine antenatal screening for HBV began17) and December 2012.

A woman was defined as having a chronic HBV infection at the delivery of her first child if there was at least one linked HBV notification in the NCIMS database that was recorded as unspecified and with a notification date earlier than the delivery date. Women with no linked HBV notifications were assumed to be not infected with HBV. Women with an HBV infection notified as being acute were excluded from the analysis, as it was unknown whether they would have cleared their acute infection or progressed to a chronic infection.

Statistical analysis

Women were categorised into four groups by their year of birth, which determined the likelihood of their being included in an HBV vaccination program: pre-vaccination era (maternal year of birth, 1981 or earlier); catch-up vaccination, predominantly GP-administered (1982–1987); at-risk newborn vaccination (1988–1991); and universal school-based catch-up and at-risk newborn vaccination (1992–1999; online Appendix 1). No women in our analyses were born during the period of universal HBV vaccination of newborns (from May 2000).

We also classified the women as Indigenous Australian, non-Indigenous Australian-born, or overseas-born women, based on their PDC record. For Indigenous status, we enhanced reporting in the PDC by linkage to other PDC records.18 Records with missing country of birth data (2090 records, 0.4% of all records) were placed in the “born overseas” category.

We calculated crude HBV prevalence for the four maternal year-of-birth categories, and used logistic regression to examine the relationship between these categories and HBV infection. We adjusted analyses for year of giving birth (in 5-year intervals) to account for possible temporal trends in HBV prevalence,2 and for the mother’s area of residence (two categories, based on residential postcode in the PDC record: major cities and regional/remote, according to the Accessibility/Remoteness Index of Australia19), as HBV prevalence in Australia varies between regions.3 The two most recent maternal year-of-birth categories (1988–1991, 1992–1999) were combined (1988–1999) for the logistic regression analysis because the numbers of records in the individual groups were small.

Ethics approval

The study was approved by the NSW Population and Health Services Research Ethics Committee (reference, 2009/11/193) and the Aboriginal Health and Medical Research Council Human Research Ethics Committee (reference, 841/12).

Results

Between January 2000 and December 2012, 482 998 women residing in NSW gave birth to their first child (PDC data); 54 were linked to an acute HBV notification and excluded from further analysis. Of the remaining 482 944 records, 11 738 (2.4%) were Indigenous Australian women, 319 629 (66.2%) were non-Indigenous Australian-born women, and 151 577 (31.4%) were born overseas. A linked unspecified HBV notification before the date of birth of their first child was available for 3383 women (HBV prevalence, 0.70%; 95% confidence interval [CI], 0.68–0.72%). HBV prevalence was estimated as 0.79% (95% CI, 0.63–0.95%) for Indigenous Australian women, 0.11% (95% CI, 0.09–0.12%) for non-Indigenous Australian-born women, and 1.95% (95% CI, 1.88–2.02%) for overseas-born women.

For Indigenous Australian women, the prevalence of HBV infection was significantly lower for those who were eligible for universal school-based or at-risk newborn vaccination (born between 1992 and 1999) than for women born during the pre-vaccination period (≤ 1981): 0.15% (95% CI, 0.00–0.35%) v 1.31% (95% CI, 0.91–1.71%; for trend, P < 0.001). For non-Indigenous Australian-born women, the prevalence also declined, but the fall was not statistically significant: from 0.10% (95% CI, 0.09–0.11%) to 0.04% (95% CI, 0.00–0.09%; for trend, P = 0.5). There was no significant trend for overseas-born women between the two periods (P = 0.1) (Box 1, online Appendix 2).

In analyses adjusted for year of giving birth and region of residence (Box 2), the proportion of Indigenous Australian women notified as having an HBV infection was 80% lower for those eligible for vaccination as part of the at-risk infant or universal school-based vaccination programs (born 1988–1999) than for women born during the pre-vaccination period (1981 or earlier) (adjusted odds ratio [aOR], 0.20; 95% CI, 0.09–0.48). There was no significant change for non-Indigenous Australian-born women (aOR, 0.87; 95% CI, 0.54–1.44). For overseas-born women, the number of notifications was significantly higher for women born during 1988–1999 than for those born before 1981 (aOR, 1.38; 95% CI, 1.15–1.67).

Box 2 also shows that HBV notifications were more frequent for Indigenous women living in regional and remote areas than for those in major cities (aOR, 2.23; 95% CI, 1.40–3.57). The opposite applied to non-Indigenous Australian-born (aOR, 0.39, 95% CI, 0.28–0.55) and overseas-born women (aOR, 0.61; 95% CI, 0.49–0.77).

The study timeframe and inclusion criteria (first births during 2000–2012) meant that the mean age of mothers was lower in later than in earlier birth year groups. After adjusting for maternal birth year groups, a significant decline in HBV notifications among Indigenous women of about 30% was still detected (aOR for each 5-year period, 0.69; 95% CI, 0.49–0.97; P = 0.03). A decline for overseas-born women was also found, but it was much smaller (aOR, 0.89; 95% CI, 0.84–0.93; P < 0.001), and there was no change for non-Indigenous Australian-born women (aOR, 0.99; 95% CI, 0.84–1.16; P = 0.90; Box 2).

To further explore the changes in HBV prevalence in overseas-born women, HBV notifications were also analysed by maternal year of birth and region of birth (Box 3). The highest proportions of women with HBV notifications were for those born in North-East Asia, South-East Asia, and sub-Saharan Africa. The small sample sizes made comparisons of trends across maternal year of birth less robust, but a consistent increase in HBV notification rates was observed for women born in North-East Asia and sub-Saharan Africa (for each trend, P < 0.001).

Discussion

This is the largest study to examine differences in HBV notification rates for women born before and after the introduction of HBV vaccination programs in Australia, analysed by country of birth, Indigenous status, and region of residence. We found that HBV notification rates for Indigenous women born after the introduction of targeted infant HBV vaccination were 80% lower than for those born earlier. For non-Indigenous Australian-born and overseas-born women there were no consistent associations between HBV notification rates and HBV vaccination programs in NSW. Despite limited data about the level of HBV vaccination coverage achieved when the at-risk newborn vaccination program was introduced in NSW in 1987, our findings suggest that it was highly successful. The estimates of HBV notification rates in Indigenous women were substantially lower among those born after 1987 than among women born before the start of the program (Box 1). It is notable that the 80% decline we report matches the 79% reduction found by a study that compared Indigenous women in the Northern Territory born before and after the introduction of universal newborn vaccination,2 suggesting that the targeted program was highly effective in reaching those at risk. The estimated fall is also similar to the results of investigations in other countries of the impact of universal newborn vaccination programs.20,21

A lack of consistent trend in HBV notifications among non-Indigenous Australian-born women might be expected, as the notification rate in this population before the introduction of vaccination was considerably lower than for Indigenous women. Further, most non-Indigenous women born during 1988–1999 would have been eligible only for school-based catch-up vaccination, which is less effective in preventing chronic disease than infant vaccination. Interpreting the relationship between birth cohorts and HBV prevalence in overseas-born women was complicated by a number of factors, including the differing prevalence of HBV in the regions from which overseas-born women migrated, their age at migration, and the lack of information about receipt of vaccination in their country of origin. When analysed by region of origin, the observed changes in notification rates could reflect either varying local uptake of infant HBV vaccination or differences in the populations that have migrated to Australia from particular regions over the 13-year study period. The smaller numbers of women involved in each group, however, limit our ability to draw conclusions.

Regional differences in HBV prevalence were also observed. Indigenous Australian women in regional and remote NSW were more likely to be HBV-seropositive than those in urban areas, whereas the reverse was true for non-Indigenous Australian-born and overseas-born women. These differences in HBV prevalence have been described previously in Indigenous Australians,2 but the reasons underlying them are unclear. The colonisation process and the institutional racial discrimination that Indigenous Australians experience affect their health outcomes, mediated by a number of different pathways, including unequal access to health care, housing and employment.22,23 As access to primary health care services relative to need is lowest in remote areas, and proportionately more Indigenous than non-Indigenous Australians live in remote areas,24 these factors may contribute to higher HBV prevalence among Indigenous women in rural and remote areas. In addition, an uncommon, more virulent HBV subgenotype circulates among Indigenous Australians in the NT, perhaps reducing the efficacy of vaccination;25 the distribution of this subgenotype in NSW, however, is unknown.

The higher prevalence of HBV among urban than regional non-Indigenous women may be related to the higher proportions of women in cities who inject drugs or are in prison, both risk factors for acute HBV infection.26 For women born overseas, the difference might be related to the fact that a greater proportion of migrants from high HBV prevalence countries (such as Asia) reside in urban than in regional and remote areas (online Appendix 3).27

It was not possible in our ecological study to take into account interactions between the effects of age and calendar year on HBV notification. Women who were born more recently, and therefore more likely to have been vaccinated, would have been younger at the time of our linkage, but also potentially subject to different risks of exposure at a given age. Including the year a woman gave birth as a factor in the regression model for Indigenous Australian women led to a small reduction in the effect of maternal birth year on HBV prevalence, and HBV prevalence was lower for more recent year of giving birth, after adjusting for maternal year of birth (Box 2). This suggests that temporal trends other than the effect of maternal birth year may have contributed to the decline in HBV notifications for Indigenous Australian women, although residual confounding related to inadequate adjustment for maternal birth year effects cannot be excluded. A similar trend, but of smaller magnitude, was seen among overseas-born women.

Antenatal screening for HBV infection enabled us to systematically assess HBV prevalence in a large population of women. Study limitations include our focus on women giving birth; our conclusions may not be generalisable to other women or to men, but we expect that the overall trends would be similar. We were unable to assess the impact of universal newborn vaccination on HBV notifications, as no women born after 2000 had given birth during the study period. Further, the ecological nature of our analyses depended on assumptions about the exposure of individuals to different vaccination strategies according to year of birth, whereas individual level vaccination data would assist us more reliably quantify their effects. Interpreting changes in HBV prevalence by country or region of birth was further limited by a lack of information about when women migrated to Australia. Some HBV notifications classified as “unspecified” may actually have been acute infections, but their frequency should not have differed between maternal birth year groups, and would therefore not have affected our estimates of HBV prevalence. Finally, linkage errors are possible, but their rate is known to be low.

Conclusion

Analysing routine antenatal HBV screening data is a simple and cost-effective method for monitoring changes in HBV prevalence in both the general population and in some high risk populations. The newborn and childhood HBV vaccination programs in NSW have had a significant impact on HBV prevalence in Indigenous Australian women, but it is still substantially higher than among non-Indigenous women. HBV infection prevention programs for high risk groups should be targeted differently, with those for Indigenous Australians focused on regional and remote NSW, and those for migrant populations on major cities. Finally, our analysis could be repeated periodically to assess the ongoing impact of universal newborn HBV vaccination and future targeted programs on HBV prevalence in Australia.

Box 1 –
Hepatitis B notifications for primiparous women giving birth, by maternal birth year, New South Wales, 2000–2012

* HBV notification rates plotted against the median maternal year of birth for each maternal year of birth category (≤ 1981, 1982–1987, 1988–1991, 1992–1999).

Box 2 –
Association between HBV notifications* and maternal year of birth, year of giving birth, and region of residence

	Median age (years)	Number of women		Univariate analysis		Multivariate analysis
	Median age (years)	Giving birth	Giving birth, with HBV record	Odds ratio (95% CI)	P^†	Adjusted odds ratio (95% CI)^‡	P^†

Australian-born women, Indigenous
Maternal year of birth
≤ 1981	27.4	3057	40 (1.3%)	1	< 0.001	1	0.002
1982–1987	20.8	4509	45 (1.0%)	0.76 (0.50–1.17)		0.79 (0.51–1.23)
1988–1999	18.8	4172	8 (0.2%)	0.15 (0.07–0.31)		0.20 (0.09–0.48)
Region of residence
Major cities		4916	24 (0.5%)	1	0.002	1	< 0.001
Regional/remote		6752	69 (1.0%)	2.08 (1.31–3.32)		2.23 (1.40–3.57)
Year of giving birth (per 5 years)				0.45 (0.34–0.61)		0.69 (0.49–0.97)	0.03
Australian-born women, non-Indigenous
Maternal year of birth
≤ 1981	30.7	227 608	227 (0.1%)	1	0.50	1	0.10
1982–1987	23.6	67 762	91 (0.1%)	1.35 (1.06–1.72)		1.47 (1.14–1.91)
1988–1999	19.9	24 259	18 (0.1%)	0.74 (0.46–1.20)		0.87 (0.54–1.44)
Region of residence
Major cities		242 392	298 (0.1%)	1	< 0.001	1	< 0.001
Regional/remote		77 195	38 (0.0%)	0.40 (0.29–0.56)		0.39 (0.28–0.55)
Year of giving birth (per 5 years)				1.04 (0.90–1.20)		0.99 (0.84–1.16)	0.90
Overseas-born women
Maternal year of birth
≤ 1981	31.7	116 659	2245 (1.9%)	1	0.10	1	0.001
1982–1987	25.2	29 431	580 (2.0%)	1.03 (0.93–1.12)		1.11 (1.01–1.22)
1988–1999	20.9	5487	129 (2.4%)	1.23 (1.03–1.47)		1.38 (1.15–1.67)
Region of residence
Major cities		144 926	2872 (2.0%)	1	< 0.001	1	< 0.001
Regional/remote		6621	82 (1.2%)	0.62 (0.50–0.77)		0.61 (0.49–0.77)
Year of giving birth (per 5 years)				0.92 (0.88–0.96)		0.89 (0.84–0.93)	< 0.001

* For the purposes of our analysis: defined as a record in the NSW Notifiable Conditions Information Management System of the detection of hepatitis B surface antigen (HBsAg) between January 1994 and December 2012 with the infection classified as being of unspecified duration (or not newly acquired). † For trend across categories of maternal birth year, calculated using the median maternal year of birth in each category. ‡ Adjusted for maternal year of birth, region of residence, and year of giving birth (5-year intervals).

Box 3 –
HBV notifications for non-Australian-born women giving birth for the first time, by region of birth

Mother’s region of birth

Maternal year of birth

≤ 1981

1982–1987

1988–1999

Number of women

Proportion with HBV record (95% CI)

Number of women

Proportion with HBV record (95% CI)

Number of women

Proportion with HBV record (95% CI)

North-East Asia

21 159

4.4% (4.2–4.7%)

4455

5.4% (4.7–6.1%)

583

11.2% (8.8–14.0%)

South-East Asia

22 824

4.3% (4.2–4.7%)

4596

4.5% (4.0–5.2%)

680

4.1% (2.9–5.9%)

Oceania (excluding Australia)

12 124

1.1% (0.9–1.2%)

3335

1.0% (0.7–1.4%)

1260

0.7% (0.4–1.4%)

Sub-Saharan Africa

4409

0.9% (0.6–1.2%)

965

3.0% (2.1–4.3%)

244

4.9% (2.8–8.4%)

North Africa or Middle East

9064

0.6% (0.5–0.8%)

4592

0.5% (0.3–0.8%)

1368

0.9% (0.5–1.5%)

South or Central Asia

12 268

0.3% (0.3–0.5%)

7292

0.4% (0.3–0.6%)

831

0.2% (0.1–0.9%)

Europe

25 899

0.2% (0.1–0.2%)

2764

0.4% (0.3–0.8%)

303

0.3% (0.1–1.9%)

Americas

7262

0.04% (0.0–0.1%)

1084

0.3% (0.1–0.8%)

126

0.0% (0.0–3.0%)

Other

1650

0.6% (0.3–1.0%)

348

0.9% (0.3–2.5%)

0.0% (0.0–4.0%)

Dengue and travellers: implications for doctors in Australia

Awareness of the problem is the first step towards control

The study by Tai and colleagues reported in this issue of the MJA highlights the risk of dengue in Australia posed by the endemic Aedes aegypti and A. albopictus vectors, together with increasing travel by Australians to dengue-endemic destinations.1 From 1991 to 2012, most cases of notified dengue in Australia were related to overseas travel, with respective increases in 2010 and 2011 of 298% and 155% above the 5-year mean notification rate; the risk of dengue in travellers returning from Indonesia between 2000 and 2011 was 8.3 times that for travellers returning from all other destinations.2 The global trade in used tyres (believed to facilitate the distribution of eggs and immature forms of mosquito vectors), rapid urbanisation in Asia and Latin America, more frequent international travel, and ineffective vector control have each contributed to the increasing global prevalence of dengue.3 It is pertinent to consider the threat of dengue in Australia with respect to travel and climatic factors.

During 1993–2005, a decrease in the average Southern Oscillation Index (that is, warmer conditions) over the preceding 3–12 months was significantly associated with increasing monthly numbers of dengue cases in Queensland.4 Sequencing data for dengue virus envelope protein genes in symptomatic travellers returning to Queensland during 2002–2010 indicated that there was an elevated risk of imported dengue associated with travel to Asia and Papua New Guinea.5

The impact of socio-ecological factors on local and imported cases of dengue should also be evaluated. A study in Queensland during 2002–2005 found that the number of patients with locally acquired dengue increased by 6% for each 1 mm increase in average monthly rainfall and by 61% for each 1°C increase in monthly maximum temperature; for imported dengue, the increase was by 1% per 1 mm increase in average monthly rainfall and 1% per single unit increase in average socio-economic index.6 A study in Cairns, 2000–2009, found that the monthly incidence of locally acquired dengue was significantly positively correlated with the monthly number of imported cases, as well as with monthly minimum temperature, monthly relative humidity, and standard deviation of daily relative humidity; it was negatively linked with monthly rainfall levels.7

However, other factors determine the risk of dengue in Australia, including human behaviour. Increased use of water storage tanks in response to drought conditions has increased the geographic distribution of A. aegypti beyond the expansion attributable to climate change.8 A dynamic life table simulation model that assessed the impact of climate change on A. aegypti distribution, based on current (1991–2011) and future (2046–2065) climate scenarios, predicted decreasing mosquito numbers in a scenario that included increasing atmospheric carbon dioxide levels and higher global temperature, but increasing mosquito abundance with more moderate increases in global carbon dioxide and temperature levels. The body weight of A. aegypti and the extrinsic incubation period of the dengue virus (ie, period between infection of the mosquito and its ability to transmit the virus) were reduced in both scenarios, and the rate of mosquito eggs deposition increased.9 Nevertheless, the probability of dengue in Australia outside northern Queensland is low according to a formal modelling framework that took into account the current distribution of dengue, rainfall, temperature, and urbanisation.10

In the absence of highly effective dengue vaccines and effective therapeutics, three elements of the global strategy for dengue prevention and control should be emphasised: surveillance for planning and response; reducing the disease burden; and changing behaviour to improve vector control.11 Dengue virus surveillance has helped mitigate dengue outbreaks in Singapore by providing early warning of impending outbreaks, allowing time to intensify vector control.12 Chemical control with larvicides and adulticide surface sprays in water stored for domestic use, and biological control agents such as larvivorous fish can be useful. Environmental management strategies include source reduction, clean-up campaigns, regular water container emptying in households and public spaces, installation of water supply systems, solid waste disposal management, and appropriate urban planning, all aimed at reducing A. aegypti breeding levels. Finally, social mobilisation through public education may enhance the effectiveness of vector control strategies.11 Promising future strategies include the introduction of genetically modified male mosquitoes that sterilise wild-type female mosquitoes, and of Wolbachia-infected A. aegypti, which are resistant to dengue infection.3

Doctors in Australia must be alert to the possibility of dengue in their differential diagnosis of febrile conditions in returned travellers. Referral for specialist opinion and confirmation of dengue virus infection by rapid diagnostic tests, such as non-structural antigen 1 assay, are appropriate when there is doubt about the diagnosis.11 Triage for admission to hospital should be based on the World Health Organization dengue guidelines,13 with particular attention to the warning signs of severe dengue. These signs were recorded for 40% of patients in the study by Tai and colleagues.1 Education of hospital doctors about these guidelines may well be needed, as the study also found that a strict fluid balance chart was not kept for 86% of the patients diagnosed and treated for dengue, 27% of patients received probably unnecessary antibiotics and blood products were administered to 15%, and potentially harmful non-steroidal anti-inflammatory drugs were prescribed for 22%.1

Death from an untreatable infection may signal the start of the post-antibiotic era

The ASID perspective on the most important infectious diseases problem of 2017 and beyond

On 12 January 2017, the United States Centers for Disease Control and Prevention reported that a woman in Nevada had died from an untreatable Gram-negative infection resistant to all available classes of antibiotics.1 The woman had sustained a fractured femur, complicated by osteomyelitis, while travelling in India, necessitating hospitalisation and intravenous antibiotic treatment. After returning to the US in mid-2016, she was admitted to hospital with systemic inflammatory response syndrome, probably secondary to a hip seroma that developed after the earlier surgery, and a pan-resistant Klebsiella pneumoniae was isolated from a tissue specimen; the woman died of untreatable septic shock.

Although infections by antimicrobial-resistant organisms are now common, we and other infectious diseases physicians, microbiologists, and public health experts in Australia and around the world are deeply alarmed by this report, as it may herald a post-antibiotic era in which high level antimicrobial resistance (AMR) is widespread, meaning that common pathogens will be untreatable. Should this be the case, it would profoundly affect all areas of health care, and society. Simple childhood infections would once again be life-threatening events, major surgery would be associated with high mortality, chemotherapy for cancer and organ transplantation would no longer be possible.

There is increasing international recognition that AMR is one of the major public health problems of our time. An independent review of AMR prepared for the United Kingdom government recommended a global public awareness campaign, reducing unnecessary antibiotic use in agriculture, and providing incentives for both AMR diagnostics and new drug development.2 The authors of the report emphasised that these goals could not be achieved without the concerted participation of the United Nations and G20 group. In September 2016, the G20 declared AMR a serious threat to public health, economic growth, and global economic stability, and called for prudent antibiotic use and action to tackle AMR.3 The UN General Assembly held a special summit later the same month at which several countries affirmed national action plans for dealing with AMR.4

The Australian government has been proactive in its response to AMR, promptly forming the Australian Antimicrobial Resistance Prevention and Containment Steering Group, led by the secretaries of the federal Departments of Health and Agriculture. Australia’s first National Antimicrobial Resistance strategy was released in June 2015, supporting a “One Health” approach to mitigating AMR (that is, recognising that human, animal and environmental health are interrelated),5 and was soon followed by an implementation plan.6 Our challenge is to translate this plan “into swift, effective, life-saving actions across the human, animal and environmental health sectors”, as the Director-General of the World Health Organization, Margaret Chan, has urged.4

The per capita consumption of antibiotics by people in Australia is among the highest in the world.7 Australian prescribers and consumers need to reduce antibiotic use in both humans and animals. The National Health and Medical Research Council National Centre for Antimicrobial Stewardship is leading national initiatives to adapt human antimicrobial stewardship to busy clinical practices in both the hospital and community settings, with the aim of improving prescribing behaviour.8 The Royal Australasian College of Physicians and the Australasian Society for Infectious Diseases (ASID) have recently developed a list of the top five low value interventions in infectious diseases,9 as discussed by Spelman and colleagues in this issue.10 Four of the five recommendations are related to reducing antibiotic use in settings where they are of limited value: asymptomatic bacteriuria, leg ulcers without clinical infection, upper respiratory tract infections, and treating faecal pathogens in the absence of diarrhoea.9 The Australian Veterinary Association has released guidelines for the prescribing of veterinary antibiotics, but antimicrobial stewardship in animals and agriculture is yet to be established.11

To have an impact on AMR, we will need to address all its drivers in Australia, including unrestrained use of antibiotics and poor infection control in both humans and animals, the decline of antibiotic research and development, and the introduction of AMR by ingesting imported food products (eg, seafood and meat) that contain AMR organisms, particularly if antibiotics were employed during their production, and through international travel. Coordination of these actions will be critical, but also complex in Australia, as health departments, antimicrobial prescribing, and communicable diseases surveillance are regulated by state-based authorities, while the federal government regulates quarantine, biosecurity, and the licensing and subsidising of medicines. The Australian Medical Association has recently called for immediate establishment of an Australian National Centre for Disease Control, “with a national focus on current and emerging communicable disease threats, engaging in global health surveillance, health security, epidemiology and research”.12 Such a body could operate in a similar manner to the European Centre for Disease Prevention and Control (ECDC), complementing and coordinating existing state- and territory-based activities.

The recent death from an untreatable infection in Nevada provides a preview of a future without effective antibiotics. A list of tangible actions against each of the drivers of AMR, coordinated across human and animal health and agriculture, must be an urgent priority. ASID, the Australian Society for Antimicrobials, and animal health societies will host government representatives and stakeholders in June 2017 at the second Australian AMR Summit in Melbourne, with the aim of drafting this action list.

Is Australia prepared for the next pandemic?

Pieces of the plan are in place, but we must continue to strengthen preparedness research capacity

Infectious diseases continue to threaten global health security,1 despite decades of advances in hygiene, vaccination and antimicrobial therapies. Population growth, widespread international travel and trade, political instability and climate change have caused rapid changes in human populations, wildlife and agriculture, in turn increasing the risk of infection transmission within and between countries and from animal species.2 New human pathogens have emerged, and previously “controlled” diseases have re-emerged or expanded their range.2 In the past decade alone, the global community has experienced infection outbreaks of pandemic influenza, Ebola and Zika viruses and Middle East respiratory syndrome (MERS).

Planning for an effective response to the next pandemic is complex and requires extensive engagement between public health experts, clinicians, diagnostic laboratory staff, general and at-risk communities and jurisdictional and federal agencies. An effective response also requires access to real-time data, management of uncertainty, clear and rapid communication, coordination and, importantly, strong leadership. Are all these pieces of the plan currently in place in Australia?

The 2009 influenza pandemic tested Australia’s capacity to respond to a highly transmissible emerging infectious disease.3 Public health units and frontline practitioners around the country were affected in different ways. The pandemic reached our states and territories at different times, leading to staggered and varied responses and pointing to clear gaps and challenges in logistics and governance. Although higher than usual rates of hospitalisation and intensive care admission, particularly among Aboriginal and Torres Strait Islander people and pregnant women, were observed early in the pandemic, most cases were mild.3 As the spectrum of disease became apparent, the existing plan, which had been based on a Spanish influenza-like worst-case scenario, was modified. The focus shifted from containing or limiting the spread of disease at a whole-of-population level to mitigation strategies targeted at key risk groups.3

Alongside their roles as primary effectors of response, frontline clinical, public health and laboratory staff were required to gather key information to inform best practice. At the same time, surge capacity was limited. Given the requirement for comprehensive laboratory testing to support diagnosis and case management in the initial phases, laboratory resources in the states affected early in the pandemic were stretched beyond their limits.4 Antivirals were available but sub-optimally deployed in some areas.4 It was therefore not possible to determine the impact of antivirals on rates of hospitalisation, the need for critical care, or death in Australia, as was reported elsewhere.5 As in other settings, the pandemic vaccine only became available after the “first wave”. However, a 20% increase in the proportion of the population with antibodies to the pandemic strain, which was associated with vaccine uptake, likely contributed to low levels of disease activity in the 2010 influenza season.6

In keeping with similar exercises globally,7 the Review of Australia’s health sector response to pandemic (H1N1) 2009 identified a need for greater flexibility in implementation plans to achieve an optimal response.4 Improved data sharing and synthesis within and between jurisdictions and internationally was defined as a key priority, to enable better understanding of the situation and evolving needs, to advise evidence-based practice and to inform clear, consistent messaging. The review also recommended development of a set of overarching ethical principles, to guide resource allocation in alignment with community expectations and values and to identify feasible interventions that are not disproportionately disruptive to society (disruptive interventions include social distancing measures such as school and workplace closures or travel restrictions). Failure to engage key populations at risk, including Aboriginal and Torres Strait Islander peoples, in preparedness activities before the 2009 pandemic was recognised as a critical deficiency.4

Much has happened since 2009. The Australian health management plan for pandemic influenza, redrafted in 2014, is a nationally agreed plan for flexible and scalable responses in the health sector. It was developed in consultation with key stakeholders, including state and territory health departments and practitioner groups involved in implementing responses.8 The plan emphasises engaging with existing committees and practitioners to provide input to decision making under the leadership of the Australian Health Protection Principal Committee (AHPPC), the key decision maker in a national health emergency. Pandemic response phases and key responsibilities in Australia, as outlined in the plan, are summarised in Box 1 and described in detail elsewhere.9 The AHPPC is advised by two expert standing committees — the Communicable Diseases Network Australia and the Public Health Laboratory Network, on which states and territories are represented by their chief health officers — and by practitioner groups including the General Practice Roundtable and National Aboriginal Community Controlled Health Organisation. The plan’s recommendations on the use of infection control measures and pharmaceuticals, including antivirals and vaccines, are based on a wealth of national and international evidence emerging from the 2009 experience.8 Corresponding efforts have gone into strengthening the National Medical Stockpile and ensuring onshore vaccine manufacturing capacity to safeguard against the emergence of novel influenza strains.

However, influenza is not the only threat to Australia’s health security. Recent outbreaks of MERS and Ebola and Zika virus infections have provided opportunities for the AHPPC and key stakeholders to practise and refine coordination and communication strategies to prevent, prepare for and respond to threats posed to Australians. These new threats highlighted the need to develop response plans that are agile, can be adapted to known and unknown pathogens and syndromes and are well coordinated with international responses. The CDPLAN: Emergency response plan for communicable disease incidents of national significance, released in September 2016, provides a generic national framework for a primary response to outbreaks for which there is no pre-existing disease-specific plan.10 This plan is supported by the National framework for communicable disease control,11 a roadmap to improve national information sharing and facilitate a coordinated response to events of public health importance.

Research readiness to identify and generate key information needed in health emergencies is also crucial. The World Health Organization’s research and development blueprint, released in May 2016, draws on lessons learned from past responses to improve preparedness and reduce the time needed to make diagnostics, therapeutics and vaccines available.12 Three main approaches are required: improved coordination and an enabling environment; acceleration of research and development processes; and new norms and standards tailored to the epidemic context.12 Both pre-emptive and responsive efforts are needed. Establishment of the Global Research Collaboration for Infectious Disease Preparedness has enabled global financial support for both. This collaboration is a network of organisations that fund research,13 of which Australia’s National Health and Medical Research Council (NHMRC) is a member.

The NHMRC has recently funded four centres of research excellence (CREs) that are focused on effective information acquisition and use, laboratory diagnostics, clinical trials, modelling and community engagement. All will contribute to Australia’s emergency response to infectious diseases (Box 2). One of these CREs, the Australian Partnership for Preparedness Research on Infectious Disease Emergencies (APPRISE), was funded under a novel paradigm in July 201614 — the requirement to complete an initial, broad stakeholder consultation to achieve an agreed research plan. Central to this consultation is the development of ethical frameworks to support implementation of an emergency response, with clear emphasis on planning with (not for) key populations, including Aboriginal and Torres Strait Islander peoples. Pre-emptive activities undertaken by the four complementary CREs will promote collaboration and information sharing between researchers, frontline responders and the community, including developing pre-approved protocols for emergency response research and implementation. This process will accelerate development and testing of novel diagnostics and therapeutic interventions; facilitate rapid acquisition, collation and interpretation of clinical and epidemiological data to support decision making; and, ultimately, enhance emergency responses.

The networks established by these CREs recognise the need for an interdisciplinary and cross-sectoral approach to preparedness research and are developing local skills and capacity to support emergency responses. Critically, they represent a focal point of engagement with similar international efforts, including PREPARE (Platform for European Preparedness against [Re-]emerging Epidemics; https://www.prepare-europe.eu) in Europe, and the REACTing (Research and action targeting emerging infectious diseases) consortium in France.15 Such links enable rapid information sharing and synthesis to inform local responses. They also facilitate participation in multinational clinical trials of sufficient power to rapidly determine effectiveness of novel infection control, therapeutic and preventive interventions, including vaccines. Equally important is the trilateral engagement between researchers, public health practitioners and policy makers in defining the research agenda. Priority needs are linked to training programs, ensuring that research activities and skills feed into ongoing policy and practice.

We are unable to predict when the next pandemic will occur or which new pathogen may appear, emphasising that every country must be well prepared. Australia has many pieces of the plan in place, but we must continue to fill gaps, test and refine existing systems and continually review what works to make sure we are as ready as possible for the next emerging infectious disease challenge. Louis Pasteur once said, “Gentlemen, it is the microbes who will have the last word”. We need to ensure that he was wrong!

Box 1 –
Pandemic response phases and key responsibilities defined by the Australian health management plan for pandemic influenza,8 superimposed on a representative epidemic curve

The AHPPC coordinates the national response under the leadership of the CMO, and the PHLN and CDNA provide critical capability to support and inform the response.

AHPPC = Australian Health Protection Principal Committee. CDNA = Communicable Diseases Network Australia. CMO = Chief Medical Officer. ED = emergency department. PHLN = Public Health Laboratory Network. WHO = World Health Organization.

Box 2 –
Current NHMRC centres of research excellence (CREs) engaged in emergency infectious diseases preparedness research*

Centre of research excellence

Stated goals

Centre of Research Excellence in Emerging Infectious Diseases (CREID)http://www.creid.org.au

Develop and integrate new technologies, including profiling the entire gene complement of microorganisms and creating new electronic communication platforms to improve the precision and speed of public health responses
Develop ethics research-based policy frameworks to enable implementation of these technologies into public health practice and policy

Centre of Research Excellence, Integrated Systems for Epidemic Response (ISER)https://sphcm.med.unsw.edu.au/centres-units/centre-research-excellence-epidemic-response

Conduct cross-sectoral collaborative research and engagement
Convene and lead multidisciplinary systems research in epidemic response across health, government, international law and security, at both national and international levels

Centre of Research Excellence in Policy Relevant Infectious Diseases Simulation and Mathematical Modelling (PRISM)http://prism.edu.au

Develop new methods for the study of disease distribution and transmission using expertise in infectious disease epidemiology, public health and mathematical and computational modelling

Australian Partnership for Preparedness Research on Infectious Disease Emergencies (APPRISE)https://www.nhmrc.gov.au/media/releases/2016/infectious-disease-emergency-response-research-funding

Support a single, multidisciplinary, nationally focused team who will establish a collaborative network to undertake infectious disease emergency response research in the Australian health system
Lead a cohesive approach to priority setting for infectious disease emergency response research
Conduct research in accordance with these priorities
Facilitate rapid Australian research responses to urgent infectious disease threats

NHMRC = National Health and Medical Research Council. * Information sourced from the NHMRC website (https://www.nhmrc.gov.au/grants-funding/research-funding-statistics-and-data), CRE websites and funding applications, where available.

Australasian Society for Infectious Diseases: low value interventions

The challenge will be changing clinicians’ behaviour and practice so that the use of low value interventions decreases

In March 2015, the Australasian Society for Infectious Diseases (ASID) was one of 41 medical societies of the Royal Australasian College of Physicians to participate in the EVOLVE initiative, aimed at identifying five practices or interventions that were of low value or of limited usefulness.1 ASID members, including paediatricians, were surveyed and asked to short-list (and rank) suggested low value interventions (LVIs). From this survey emerged an overall short list that was circulated to respondents for further comment, and the final five LVIs were submitted to the ASID Council for endorsement.1

We present these five interventions below, with rationales as to why they are considered to be of low value. There are, of course, some uncommon situations where these interventions may demonstrate utility and we give some examples of these exceptions.

It is notable that four of the five interventions relate to the inappropriate use of antibiotics. Antibiotic use, both appropriate and inappropriate, is the major driver of antimicrobial resistance, which a recent World Health Organization report has highlighted as “an increasingly serious threat to global public health”.2 Inappropriate antibiotic use is also associated with a risk of Clostridium difficile infection,3 an unnecessary risk of developing antibiotic allergy and unjustified health care costs.

The five low value interventions

1. Prescribing antibiotics for asymptomatic bacteriuria

Asymptomatic bacteriuria (with or without pyuria) is common, particularly in older patients, and does not require treatment. Antibiotic treatment for asymptomatic bacteriuria does not decrease the incidence of symptomatic urinary tract infection or systemic sepsis. This also applies to patients with indwelling catheters: bacteriuria is almost universal in patients with urinary catheters in situ for more than a few days, and antimicrobial therapy does not decrease their risk of clinical symptoms or sepsis.

Thus, it is generally recommended that clinicians request urine samples for microscopy and culture only when patients have symptoms. Because a positive urine culture from an asymptomatic patient may trigger a decision to prescribe unnecessary antibiotic therapy, not ordering the test is the best way to avoid this situation. There are a few situations where antibiotics are indicated for asymptomatic bacteriuria. The most common are during pregnancy,4 when screening should be performed at the first antenatal visit,3 and preoperatively for patients undergoing a urological procedure in which mucosal bleeding is anticipated.4

2. Taking a swab of a leg ulcer without signs of clinical infection and treating the patient with antibiotics against the identified bacteria

Leg ulcers, such as venous ulcers, should not be investigated or treated for bacterial infection in the absence of clinical evidence of infection, such as purulent discharge or spreading erythema. There is no evidence that antibiotic therapy promotes wound healing in this setting5 Swabbing an ulcer and performing microscopy and culture in the absence of clinical signs of infection may identify commensal flora of no clinical relevance. Even if a potential pathogen such as Staphylococcus aureus or a β-haemolytic streptococcus is present, antimicrobial therapy in the absence of significant inflammation is not recommended. These recommendations for leg ulcers (not to take a swab or treat with antibiotics unless there are clinical symptoms of infection) apply to many other skin conditions that may present with leg erythema, such as lower leg venous stasis, contact dermatitis, arterial ischaemia and dependent oedema.

3. Treating upper respiratory tract infections with antibiotics

Most uncomplicated upper respiratory tract infections (URTIs) are viral in aetiology and antibiotic therapy is not indicated. This is particularly relevant in young children, who frequently receive unnecessary antibiotic therapy for URTIs. The antibiotic volume of the Australian Therapeutic Guidelines recommends avoiding “routine use” of antibiotic therapy for acute rhinosinusitis.3 Antibiotics are frequently prescribed for a purulent nasal discharge or to prevent secondary bacterial pneumonia,6 but there is no evidence to support such use.

Symptomatic management and education about the lack of benefit and potential adverse effects of antibiotics are key in this setting. Education can change doctors’ behaviour with regard to inappropriate prescribing of antibiotics,7 and education for patients and their parents or caregivers should help them to understand that improvement in the patient’s condition came with time and not as a result of inappropriately prescribed antibiotics.

There are specific URTIs where antibiotics are indicated, and these include Streptococcus pyogenes pharyngitis and Bordetella pertussis infection.

4. Investigation for faecal pathogens in the absence of diarrhoea or other gastrointestinal symptoms

Microscopy and culture or, more recently (and particularly), multiplex polymerase chain reaction (PCR) testing of faeces, should not be performed in the absence of diarrhoea or other gastrointestinal symptoms. Microbiology laboratories should not process a formed faecal specimen. Moreover, antimicrobial treatment for a potential gastrointestinal pathogen is not indicated in the absence of symptoms. For example, a patient whose diarrhoea has resolved by the time a microbiological diagnosis of C. difficile infection is made does not require treatment.

The recent introduction of faecal multiplex DNA-based diagnostic (PCR) methods has resulted in increased detection and reporting of several rarely pathogenic protozoa, especially Blastocystis hominis and Dientamoeba fragilis, as molecular methods are considerably more sensitive than microscopy. These organisms are often found in patients who are asymptomatic or whose symptoms are incompatible with enteric infection. Antimicrobial treatment is generally unnecessary and not recommended. The Australian and New Zealand Paediatric Infectious Diseases Group has highlighted this issue8 and, following consultation, the Royal College of Pathologists of Australasia now recommends that diagnostic laboratories use multiplex PCR tests without targets for these two protozoans.9

There are times where testing of non-diarrhoea stool may be indicated. These include:

screening of refugees for chronic parasitic infection that may be asymptomatic (eg, schistosomiasis and strongyloidosis);10
neurological syndromes (eg, acute flaccid paralysis) where enteroviruses may be implicated on epidemiological grounds;11 and
to confirm faecal clearance of Salmonella typhi or Salmonella paratyphi after treatment of enteric fever in food handlers, under the direction of public health authorities.

5. Ordering multiple serological investigations for patients with fatigue without a clinical indication or relevant epidemiology

It is very unusual for serological testing (eg, for brucellosis, Q fever, rickettsial disease, syphilis) to identify an underlying cause of fatigue if there is no clinical indication of an infectious cause on history or examination and in the absence of relevant epidemiology (ie, known risk factors).12 This is especially true if the patient has been fatigued for a prolonged period.

Acute (IgM) serological testing is notoriously non-specific and often leads to further unnecessary investigations and treatments, with potential adverse effects, inconvenience, erroneous diagnoses (eg, in the case of false positive results) and cost.

Use of low value interventions

Although there are no national data on how often the LVIs described above are used in current clinical practice, some studies suggest they are likely to be widespread. In one report from New Zealand, more than three-quarters of patients with an URTI received antibiotics.13

The underlying reasons for the popularity of these interventions are multiple and include: lack of an evidence base for treating some conditions; the expectations of patients and caregivers;14 suboptimal training and work pressure for clinicians;15 the anxiety of missing the diagnosis of a significant condition;16 and fear of litigation.15 Broad spectrum testing and therapy may be perceived (almost always erroneously) to compensate in some way for the lack of an evidence base.14

The EVOLVE initiative continues to be a useful vehicle to question common but non-evidence-based and potentially wasteful and harmful clinical practices, and to identify and discuss interventions that are of low value. However, the lack of usefulness of many of these LVIs is already well known, so it is important to question why they are still being used.

The challenge for ASID, and for all the societies involved in the EVOLVE initiative, is influencing behaviour to change practice so that the use of identified LVIs by medical practitioners decreases. Widespread and ongoing education, directed both at practitioners and the community, should be enhanced. ASID’s participation in the expert working groups that develop the antibiotic volume of the Australian Therapeutic Guidelines3 is likely to influence inappropriate antimicrobial prescribing because these guidelines are evidence-based and widely used.

Antimicrobial stewardship activities in hospitals do decrease inappropriate antibiotic use,17 and this may provide lessons for changing practice in the broader medical community. Finally, change may also be driven by incentives linked to best practice and by alterations to the regulatory environment, such as may come from the Medical Benefits Scheme Review.18

Impact of overweight and obesity as a risk factor for chronic conditions

This report updates and extends estimates of the burden due to overweight and obesity reported in the Australian Burden of Disease Study 2011 to include burden in people aged under 25, revised diseases linked to overweight and obesity based on the latest evidence, and estimates by socioeconomic group. The report includes scenario modelling, undertaken to assess the potential impact on future health burden if overweight and obesity in the population continues to rise or is reduced. The enhanced analysis in the report shows that 7.0% of the total health burden in Australia in 2011 is due to overweight and obesity, and that this burden increased with increasing level of socioeconomic disadvantage.

JOSEPH PRIESTLEY AND A BOTTLE OF POP

PROFESSOR STEPHEN LEEDER, EMERITUS PROFESSOR PUBLIC HEALTH, UNIVERSITY OF SYDNEY

A South African friend, passionate about finding effective ways of combatting obesity worldwide, recently sent me a clipping from The Yorkshire Evening Post of March 22, titled ‘How fizzy drinks were invented in Leeds on this day 250 years ago’.

The inventor was Joseph Priestley, the quirky theologian and polymath who had discovered oxygen years earlier.

Priestley came to live next door to a Leeds brewery, in which he took an inquisitive interest. He found that the gas given off by fermenting beer, which he called ‘fixed air’ to distinguish it from ordinary air, while toxic to mice, could be dissolved in water, giving it an agreeable flavour. He served the water to his friends, who liked it. And then, in the late eighteenth century, the Swiss J J Schweppe developed a large-scale process to carbonate water.

Today our concern with fizzy drinks is mainly with their huge sugar content and sugar’s contribution, the world over, to weight gain. With several countries introducing a sugar tax, such a tax is being considered here.

But as Linda Cobiac, King Tam, Lenner Veeman and Tony Blakely wrote in a paper in PLOS Medicine recently, ‘the cost-effectiveness of combining taxes on unhealthy foods and subsidies on healthy foods is not well understood’. Cobiac and colleagues are public health and health policy professionals in Melbourne, Brisbane, and Wellington, NZ.

They have developed a complex model of prices, relationships of salt, fat, sugar and fresh vegetables to disease states, and have used data from several countries about what could be achieved by taxing or subsidising certain foods.

Their simulations showed that ‘the combination of taxes and subsidy could avert as many as 470,000 disability-adjusted life years (that is, loss of life due to premature death and discounted years due to illness) in Australia’s 22 million people with a net saving [yes, a SAVING!] of $3.4 billion a year’.

I have a message for those who tell us that the costs of health care in Australia are unsustainable. If you want to save money, here are some approaches that could be tried – and confirmed or refuted by experimentation. This is an important caveat given that models are not the same as RCTs.

But this experimentation is surely better than trying to save health dollars by coordinating care, for patients with serious and continuing illness, between hospital and home – a demonstrably worthwhile thing to do – but which, because of the needs it uncovers, inevitably ends up costing more than standard fragmented care.

The authors draw a quiet and modest conclusion. “With potentially large health benefits for the Australian population and large benefits reducing health sector spending on the treatment of non-communicable diseases, the formulation of a tax and subsidy package should be given a more prominent role in Australia’s public health strategy.”

Their approach might seem unorthodox, but I can imagine that Priestley, the radical preacher, might be supportive. His beliefs cost him a berth as science adviser on Cook’s second voyage. He and his family, by fleeing to Pennsylvania, only just escaped death for their unorthodox theology.

He was a critical thinker and explorer. I fancy that, were he with us today, he might have encouraged us to try this out.