The 2023 report of the MJA-Lancet Countdown on health and climate change: sustainability needed in Australia's health care sector.

The MJA-Lancet Countdown on health and climate change in Australia was established in 2017 and produced its first national assessment in 2018 and annual updates in 2019, 2020, 2021 and 2022. It examines five broad domains: health hazards, exposures and impacts; adaptation, planning and resilience for health; mitigation actions and health co-benefits; economics and finance; and public and political engagement. In this, the sixth report of the MJA-Lancet Countdown, we track progress on an extensive suite of indicators across these five domains, accessing and presenting the latest data and further refining and developing our analyses. Our results highlight the health and economic costs of inaction on health and climate change. A series of major flood events across the four eastern states of Australia in 2022 was the main contributor to insured losses from climate-related catastrophes of $7.168 billion - the highest amount on record. The floods also directly caused 23 deaths and resulted in the displacement of tens of thousands of people. High red meat and processed meat consumption and insufficient consumption of fruit and vegetables accounted for about half of the 87 166 diet-related deaths in Australia in 2021. Correction of this imbalance would both save lives and reduce the heavy carbon footprint associated with meat production. We find signs of progress on health and climate change. Importantly, the Australian Government released Australia's first National Health and Climate Strategy, and the Government of Western Australia is preparing a Health Sector Adaptation Plan. We also find increasing action on, and engagement with, health and climate change at a community level, with the number of electric vehicle sales almost doubling in 2022 compared with 2021, and with a 65% increase in coverage of health and climate change in the media in 2022 compared with 2021. Overall, the urgency of substantial enhancements in Australia's mitigation and adaptation responses to the enormous health and climate change challenge cannot be overstated. Australia's energy system, and its health care sector, currently emit an unreasonable and unjust proportion of greenhouse gases into the atmosphere. As the Lancet Countdown enters its second and most critical phase in the leadup to 2030, the depth and breadth of our assessment of health and climate change will be augmented to increasingly examine Australia in its regional context, and to better measure and track key issues in Australia such as mental health and Aboriginal and Torres Strait Islander health and wellbeing.

Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling.

Activation of NADPH oxidase (NOX) enzymes and the generation of reactive oxygen species and oxidative stress regulate vascular and renal function and contribute to the pathogenesis of hypertension. The present study examined the role of NOXA1/NOX1 function in vascular reactivity of renal and mesenteric resistance arteries/arterioles of wild-type and Noxa1-/- mice. A major finding was that renal blood flow is less sensitive to acute stimulation by angiotensin II (ANG II) in Noxa1-/- mice compared with wild-type mice, with a direct action on resistance arterioles independent of nitric oxide (NO) bioavailability. These functional results were reinforced by immunofluorescence evidence of NOXA1/NOX1 protein presence in renal arteries, afferent arterioles, and glomeruli as well as their upregulation by ANG II. In contrast, the renal vascular response to the thromboxane mimetic U46619 was effectively blunted by NO and was similar in both mouse genotypes and thus independent of NOXA1/NOX1 signaling. However, phenylephrine- and ANG II-induced contraction of isolated mesenteric arteries was less pronounced and buffering of vasoconstriction after acetylcholine and nitroprusside stimulation was reduced in Noxa1-/- mice, suggesting endothelial NO-dependent mechanisms. An involvement of NOXA1/NOX1/O2•- signaling in response to ANG II was demonstrated with the specific NOXA1/NOX1 assembly inhibitor C25 and the nonspecific NOX inhibitor diphenyleneiodonium chloride in cultured vascular smooth muscle cells and isolated mesenteric resistance arteries. Collectively, our data indicate that the NOX1/NOXA1/O2•- pathway contributes to acute vasoconstriction induced by ANG II in renal and mesenteric vascular beds and may contribute to ANG II-induced hypertension.NEW & NOTEWORTHY Renal reactivity to angiotensin II (ANG II) is mediated by superoxide signaling produced by NADPH oxidase (NOX)A1/NOX1. Acute vasoconstriction of renal arteries by ANG was blunted in Noxa1-/- compared with wild-type mice. NOXA1/NOX1/O2•- signaling was also observed in ANG II stimulation of vascular smooth muscle cells and isolated mesenteric resistance arteries, indicating that it contributes to ANG II-induced hypertension. A NOXA1/NOX1 assembly inhibitor (C25) has been characterized that inhibits superoxide production and ameliorates the effects of ANG II.

Ap2s1 mutation causes hypercalcaemia in mice and impairs interaction between calcium-sensing receptor and adaptor protein-2.

Adaptor protein 2 (AP2), a heterotetrameric complex comprising AP2α, AP2ß2, AP2µ2 and AP2σ2 subunits, is ubiquitously expressed and involved in endocytosis and trafficking of membrane proteins, such as the calcium-sensing receptor (CaSR), a G-protein coupled receptor that signals via Gα11. Mutations of CaSR, Gα11 and AP2σ2, encoded by AP2S1, cause familial hypocalciuric hypercalcaemia types 1-3 (FHH1-3), respectively. FHH3 patients have heterozygous AP2S1 missense Arg15 mutations (p.Arg15Cys, p.Arg15His or p.Arg15Leu) with hypercalcaemia, which may be marked and symptomatic, and occasional hypophosphataemia and osteomalacia. To further characterize the phenotypic spectrum and calcitropic pathophysiology of FHH3, we used CRISPR/Cas9 genome editing to generate mice harboring the AP2S1 p.Arg15Leu mutation, which causes the most severe FHH3 phenotype. Heterozygous (Ap2s1+/L15) mice were viable, and had marked hypercalcaemia, hypermagnesaemia, hypophosphataemia, and increases in alkaline phosphatase activity and fibroblast growth factor-23. Plasma 1,25-dihydroxyvitamin D was normal, and no alterations in bone mineral density or bone turnover were noted. Homozygous (Ap2s1L15/L15) mice invariably died perinatally. Co-immunoprecipitation studies showed that the AP2S1 p.Arg15Leu mutation impaired protein-protein interactions between AP2σ2 and the other AP2 subunits, and also with the CaSR. Cinacalcet, a CaSR positive allosteric modulator, decreased plasma calcium and parathyroid hormone concentrations in Ap2s1+/L15 mice, but had no effect on the diminished AP2σ2-CaSR interaction in vitro. Thus, our studies have established a mouse model that is representative for FHH3 in humans, and demonstrated that the AP2S1 p.Arg15Leu mutation causes a predominantly calcitropic phenotype, which can be ameliorated by treatment with cinacalcet.

Acculturation and risk of traffic crashes in young Asian-born Australian drivers.

The study examines changes over time in crash risk differences between young Australian drivers born in Asia and those born in Australia.Data from the 2003 baseline survey of the DRIVE cohort of 20 806 young drivers aged 17-24 years were linked to police, hospital and death data up until 2016. The association between country of birth and crash was investigated using flexible parametric survival models adjusted for confounders.Six months after baseline, the crash risk in Asian-born drivers was less than half that of their Australian-born counterparts (mean HR, MHR 0.41; 95% CI 0.29 to 0.57), only to increase steadily over time to resemble that of Australian-born drivers 13 years later (MHR 0.94; 95% CI 0.66 to 1.36).This is likely to be associated with acculturation and the adoption by young Asian-born Australian drivers of driving behaviour patterns akin to those born locally. This needs to be considered in future road safety campaigns.

Self-harm in adolescence and risk of crash: a 13-year cohort study of novice drivers in New South Wales, Australia.

INTRODUCTION: Self-harm and suicide are leading causes of morbidity and death for young people, worldwide. Previous research has identified self-harm is a risk factor for vehicle crashes, however, there is a lack of long-term crash data post licensing that investigates this relationship. We aimed to determine whether adolescent self-harm persists as crash risk factor in adulthood. METHODS: We followed 20 806 newly licensed adolescent and young adult drivers in the DRIVE prospective cohort for 13 years to examine whether self-harm was a risk factor for vehicle crashes. The association between self-harm and crash was analysed using cumulative incidence curves investigating time to first crash and quantified using negative binominal regression models adjusted for driver demographics and conventional crash risk factors. RESULTS: Adolescents who reported self-harm at baseline were at increased risk of crashes 13 years later than those reporting no self-harm (relative risk (RR) 1.29: 95% CI 1.14 to 1.47). This risk remained after controlling for driver experience, demographic characteristics and known risk factors for crashes, including alcohol use and risk taking behaviour (RR 1.23: 95% CI 1.08 to 1.39). Sensation seeking had an additive effect on the association between self-harm and single-vehicle crashes (relative excess risk due to interaction 0.87: 95% CI 0.07 to 1.67), but not for other types of crashes. DISCUSSION: Our findings add to the growing body of evidence that self-harm during adolescence predicts a range of poorer health outcomes, including motor vehicle crash risks that warrant further investigation and consideration in road safety interventions. Complex interventions addressing self-harm in adolescence, as well as road safety and substance use, are critical for preventing health harming behaviours across the life course.

FEEDBACK trial - A randomised control trial to investigate the effect of personalised feedback and financial incentives on reducing the incidence of road crashes.

BACKGROUND: Road crashes continue to pose a significant threat to global health. Young drivers aged between 18 and 25 are over-represented in road injury and fatality statistics, especially the first six months after obtaining their license. This study is the first multi-centre two-arm parallel-group individually randomised controlled trial (the FEEDBACK Trial) that will examine whether the delivery of personalised driver feedback plus financial incentives is superior to no feedback and no financial incentives in reducing motor vehicle crashes among young drivers (18 to 20 years) during the first year of provisional licensing. METHODS: A total of 3,610 young drivers on their provisional licence (P1, the first-year provisional licensing) will participate in the trial over 28 weeks, including a 4-week baseline, 20-week intervention and 4-week post-intervention period. The primary outcome of the study will be police-reported crashes over the 20-week intervention period and the 4-week post-intervention period. Secondary outcomes include driving behaviours such as speeding and harsh braking that contribute to road crashes, which will be attained weekly from mobile telematics delivered to a smartphone app. DISCUSSION: Assuming a positive finding associated with personalised driver feedback and financial incentives in reducing road crashes among young drivers, the study will provide important evidence to support policymakers in introducing the intervention(s) as a key strategy to mitigate the risks associated with the burden of road injury among this vulnerable population. TRIAL REGISTRATION: Registered under the Australian New Zealand Clinical Trials Registry (ANZCTR) - ACTRN12623000387628p on April 17, 2023.

Validation of an Indirect Immunofluorescence Assay and Commercial Q Fever Enzyme-Linked Immunosorbent Assay for Use in Macropods.

Kangaroos are considered to be an important reservoir of Q fever in Australia, although there is limited knowledge on the true prevalence and distribution of coxiellosis in Australian macropod populations. Serological tests serve as useful surveillance tools, but formal test validation is needed to be able to estimate true seroprevalence rates, and few tests have been validated to screen wildlife species for Q fever. In this study, we modified and optimized a phase-specific indirect immunofluorescence assay (IFA) for the detection of IgG antibodies against Coxiella burnetii in macropod sera. The assay was validated against the commercially available ID Screen Q fever indirect multispecies enzyme-linked immunosorbent assay (ELISA) kit (IDVet, Grabels, France) to estimate the diagnostic sensitivity and specificity of each assay, using Bayesian latent class analysis. A direct comparison of the two tests was performed by testing 303 serum samples from 10 macropod populations from the east coast of Australia and New Zealand. The analysis indicated that the IFA had relatively high diagnostic sensitivity (97.6% [95% credible interval [CrI], 88.0 to 99.9]) and diagnostic specificity (98.5% [95% CrI, 94.4 to 99.9]). In comparison, the ELISA had relatively poor diagnostic sensitivity (42.1% [95% CrI, 33.7 to 50.8]) and similar diagnostic specificity (99.2% [95% CrI, 96.4 to 100]) using the cutoff values recommended by the manufacturer. The estimated true seroprevalence of C. burnetii exposure in the macropod populations included in this study ranged from 0% in New Zealand and Victoria, Australia, up to 94.2% in one population from New South Wales, Australia.

The 2022 report of the MJA-Lancet Countdown on health and climate change: Australia unprepared and paying the price.

The MJA-Lancet Countdown on health and climate change in Australia was established in 2017 and produced its first national assessment in 2018 and annual updates in 2019, 2020 and 2021. It examines five broad domains: climate change impacts, exposures and vulnerability; adaptation, planning and resilience for health; mitigation actions and health co-benefits; economics and finance; and public and political engagement. In this, the fifth year of the MJA-Lancet Countdown, we track progress on an extensive suite of indicators across these five domains, accessing and presenting the latest data and further refining and developing our analyses. Within just two years, Australia has experienced two unprecedented national catastrophes - the 2019-2020 summer heatwaves and bushfires and the 2021-2022 torrential rains and flooding. Such events are costing lives and displacing tens of thousands of people. Further, our analysis shows that there are clear signs that Australia's health emergency management capacity substantially decreased in 2021. We find some signs of progress with respect to health and climate change. The states continue to lead the way in health and climate change adaptation planning, with the Victorian plan being published in early 2022. At the national level, we note progress in health and climate change research funding by the National Health and Medical Research Council. We now also see an acceleration in the uptake of electric vehicles and continued uptake of and employment in renewable energy. However, we also find Australia's transition to renewables and zero carbon remains unacceptably slow, and the Australian Government's continuing failure to produce a national climate change and health adaptation plan places the health and lives of Australians at unnecessary risk today, which does not bode well for the future.

The 2021 report of the MJA-Lancet Countdown on health and climate change: Australia increasingly out on a limb.

The MJA-Lancet Countdown on health and climate change in Australia was established in 2017, and produced its first national assessment in 2018, its first annual update in 2019, and its second annual update in 2020. It examines indicators across five broad domains: climate change impacts, exposures and vulnerability; adaptation, planning and resilience for health; mitigation actions and health co-benefits; economics and finance; and public and political engagement. Our special report in 2020 focused on the unprecedented and catastrophic 2019-20 Australian bushfire season, highlighting indicators that explore the relationships between health, climate change and bushfires. For 2021, we return to reporting on the full suite of indicators across each of the five domains and have added some new indicators. We find that Australians are increasingly exposed to and vulnerable to excess heat and that this is already limiting our way of life, increasing the risk of heat stress during outdoor sports, and decreasing work productivity across a range of sectors. Other weather extremes are also on the rise, resulting in escalating social, economic and health impacts. Climate change disproportionately threatens Indigenous Australians' wellbeing in multiple and complex ways. In response to these threats, we find positive action at the individual, local, state and territory levels, with growing uptake of rooftop solar and electric vehicles, and the beginnings of appropriate adaptation planning. However, this is severely undermined by national policies and actions that are contrary and increasingly place Australia out on a limb. Australia has responded well to the COVID-19 public health crisis (while still emerging from the bushfire crisis that preceded it) and it now needs to respond to and prepare for the health crises resulting from climate change.

Whole genome sequence analysis identifies a PAX2 mutation to establish a correct diagnosis for a syndromic form of hyperuricemia.

Hereditary hyperuricemia may occur as part of a syndromic disorder or as an isolated nonsyndromic disease, and over 20 causative genes have been identified. Here, we report the use of whole genome sequencing (WGS) to establish a diagnosis in a family in which individuals were affected with gout, hyperuricemia associated with reduced fractional excretion of uric acid, chronic kidney disease (CKD), and secondary hyperparathyroidism, that are consistent with familial juvenile hyperuricemic nephropathy (FJHN). However, single gene testing had not detected mutations in the uromodulin (UMOD) or renin (REN) genes, which cause approximately 30-90% of FJHN. WGS was therefore undertaken, and this identified a heterozygous c.226G>C (p.Gly76Arg) missense variant in the paired box gene 2 (PAX2) gene, which co-segregated with renal tubulopathy in the family. PAX2 mutations are associated with renal coloboma syndrome (RCS), which is characterized by abnormalities in renal structure and function, and anomalies of the optic nerve. Ophthalmological examination in two adult brothers affected with hyperuricemia, gout, and CKD revealed the presence of optic disc pits, consistent with optic nerve coloboma, thereby revising the diagnosis from FJHN to RCS. Thus, our results demonstrate the utility of WGS analysis in establishing the correct diagnosis in disorders with multiple etiologies.

Benthic-pelagic coupling in the Barents Sea: an integrated data-model framework.

The Barents Sea is experiencing long-term climate-driven changes, e.g. modification in oceanographic conditions and extensive sea ice loss, which can lead to large, yet unquantified disruptions to ecosystem functioning. This key region hosts a large fraction of Arctic primary productivity. However, processes governing benthic and pelagic coupling are not mechanistically understood, limiting our ability to predict the impacts of future perturbations. We combine field observations with a reaction-transport model approach to quantify organic matter (OM) processing and disentangle its drivers. Sedimentary OM reactivity patterns show no gradients relative to sea ice extent, being mostly driven by seafloor spatial heterogeneity. Burial of high reactivity, marine-derived OM is evident at sites influenced by Atlantic Water (AW), whereas low reactivity material is linked to terrestrial inputs on the central shelf. Degradation rates are mainly driven by aerobic respiration (40-75%), being greater at sites where highly reactive material is buried. Similarly, ammonium and phosphate fluxes are greater at those sites. The present-day AW-dominated shelf might represent the future scenario for the entire Barents Sea. Our results represent a baseline systematic understanding of seafloor geochemistry, allowing us to anticipate changes that could be imposed on the pan-Arctic in the future if climate-driven perturbations persist. This article is part of the theme issue 'The changing Arctic Ocean: consequences for biological communities, biogeochemical processes and ecosystem functioning'.

Does Arctic warming reduce preservation of organic matter in Barents Sea sediments?

Over the last few decades, the Barents Sea experienced substantial warming, an expansion of relatively warm Atlantic water and a reduction in sea ice cover. This environmental change forces the entire Barents Sea ecosystem to adapt and restructure and therefore changes in pelagic-benthic coupling, organic matter sedimentation and long-term carbon sequestration are expected. Here we combine new and existing organic and inorganic geochemical surface sediment data from the western Barents Sea and show a clear link between the modern ecosystem structure, sea ice cover and the organic carbon and CaCO3 contents in Barents Sea surface sediments. Furthermore, we discuss the sources of total and reactive iron phases and evaluate the spatial distribution of organic carbon bound to reactive iron. Consistent with a recent global estimate we find that on average 21.0 ± 8.3 per cent of the total organic carbon is associated to reactive iron (fOC-FeR) in Barents Sea surface sediments. The spatial distribution of fOC-FeR, however, seems to be unrelated to sea ice cover, Atlantic water inflow or proximity to land. Future Arctic warming might, therefore, neither increase nor decrease the burial rates of iron-associated organic carbon. However, our results also imply that ongoing sea ice reduction and the associated alteration of vertical carbon fluxes might cause accompanied shifts in the Barents Sea surface sedimentary organic carbon content, which might result in overall reduced carbon sequestration in the future. This article is part of the theme issue 'The changing Arctic Ocean: consequences for biological communities, biogeochemical processes and ecosystem functioning'.

Transformation of organic matter in a Barents Sea sediment profile: coupled geochemical and microbiological processes.

Process-based, mechanistic investigations of organic matter transformation and diagenesis directly beneath the sediment-water interface (SWI) in Arctic continental shelves are vital as these regions are at greatest risk of future change. This is in part due to disruptions in benthic-pelagic coupling associated with ocean current change and sea ice retreat. Here, we focus on a high-resolution, multi-disciplinary set of measurements that illustrate how microbial processes involved in the degradation of organic matter are directly coupled with inorganic and organic geochemical sediment properties (measured and modelled) as well as the extent/depth of bioturbation. We find direct links between aerobic processes, reactive organic carbon and highest abundances of bacteria and archaea in the uppermost layer (0-4.5 cm depth) followed by dominance of microbes involved in nitrate/nitrite and iron/manganese reduction across the oxic-anoxic redox boundary (approx. 4.5-10.5 cm depth). Sulfate reducers dominate in the deeper (approx. 10.5-33 cm) anoxic sediments which is consistent with the modelled reactive transport framework. Importantly, organic matter reactivity as tracked by organic geochemical parameters (n-alkanes, n-alkanoic acids, n-alkanols and sterols) changes most dramatically at and directly below the SWI together with sedimentology and biological activity but remained relatively unchanged across deeper changes in sedimentology. This article is part of the theme issue 'The changing Arctic Ocean: consequences for biological communities, biogeochemical processes and ecosystem functioning'.

The 2019 report of the MJA-Lancet Countdown on health and climate change: a turbulent year with mixed progress.

The MJA-Lancet Countdown on health and climate change was established in 2017 and produced its first Australian national assessment in 2018. It examined 41 indicators across five broad domains: climate change impacts, exposures and vulnerability; adaptation, planning and resilience for health; mitigation actions and health co-benefits; economics and finance; and public and political engagement. It found that, overall, Australia is vulnerable to the impacts of climate change on health, and that policy inaction in this regard threatens Australian lives. In this report we present the 2019 update. We track progress on health and climate change in Australia across the same five broad domains and many of the same indicators as in 2018. A number of new indicators are introduced this year, including one focused on wildfire exposure, and another on engagement in health and climate change in the corporate sector. Several of the previously reported indicators are not included this year, either due to their discontinuation by the parent project, the Lancet Countdown, or because insufficient new data were available for us to meaningfully provide an update to the indicator. In a year marked by an Australian federal election in which climate change featured prominently, we find mixed progress on health and climate change in this country. There has been progress in renewable energy generation, including substantial employment increases in this sector. There has also been some progress at state and local government level. However, there continues to be no engagement on health and climate change in the Australian federal Parliament, and Australia performs poorly across many of the indicators in comparison to other developed countries; for example, it is one of the world's largest net exporters of coal and its electricity generation from low carbon sources is low. We also find significantly increasing exposure of Australians to heatwaves and, in most states and territories, continuing elevated suicide rates at higher temperatures. We conclude that Australia remains at significant risk of declines in health due to climate change, and that substantial and sustained national action is urgently required in order to prevent this.

Evidence for the 'safety in density' effect for cyclists: validation of agent-based modelling results.

The safety in numbers (SiN) effect for cyclists is widely observed but remains poorly understood. Although most studies investigating the SiN phenomenon have focused on behavioural adaptation to 'numbers' of cyclists in the road network, previous work in simulated environments has suggested SiN may instead be driven by increases in local cyclist spatial density, which prevents drivers from attempting to move through groups of oncoming cyclists. This study therefore set out to validate the results of prior simulation studies in a real-world environment. Time-gap analysis of cyclists passing through an intersection was conducted using 5 hours of video observation of a single intersection in the city of Melbourne, Australia, where motorists were required to 'yield' to oncoming cyclists. Results demonstrated that potential collisions between motor vehicles and cyclists reduced with increasing cyclists per minute passing through the intersection. These results successfully validate those observed under simulated conditions, supporting evidence of a proposed causal mechanism related to safety in density rather than SiN, per se. Implications of these results for transportation planners, cyclists and transportation safety researchers are discussed, suggesting that increased cyclist safety could be achieved through directing cyclists towards focused, strategic corridors rather than dispersed across a network.

Crash characteristics of on-road single-bicycle crashes: an under-recognised problem.

Compared with crashes with motor vehicles, single-bicycle crashes are an under-recognised contributor to cycling injury and the aetiology is poorly understood. Using an in-depth crash investigation technique, this study describes the crash characteristics and patient outcomes of a sample of cyclists admitted to hospital following on-road bicycle crashes. Enrolled cyclists completed a structured interview, and injury details and patient outcomes were extracted from trauma registries. Single-bicycle crashes (n=62) accounted for 48% of on-road crashes and commonly involved experienced cyclists. Common single-bicycle crash types included loss-of-control events, interactions with tram tracks, striking potholes or objects or resulting from mechanical issues with the bicycle. To address single-bicycle crashes, targeted countermeasures are required for each of these specific crash types.

Traditional Salmonella Typhimurium typing tools (phage typing and MLVA) are sufficient to resolve well-defined outbreak events only.

Between 1991 and 2014 the per capita notification rate of salmonellosis in Australia increased from 31.9 to 69.7 cases per 100,000 people. Salmonella Typhimurium accounted for nearly half the human cases until the end of 2014. In this study, we used cluster analysis tools to compare S. Typhimurium isolates from a chicken-meat study with those reported to the National Enteric Pathogen Surveillance System (NEPSS) from the coincident human and non-human populations. There was limited phage type diversity within all populations and a lack of specificity of MLVA profiling within phage types. The chicken-meat study isolates were not significantly clustered with the human cases and at least 7 non-human sources, based on typing profiles (PT/MLVA combination), could be implicated as a source of human cases during the same period. In the absence of a strong surveillance system representative of all putative sources, MLVA and phage typing alone or in combination are insufficient to identify the source of human cases.

Epidemiology of gastrointestinal nematodes of alpacas in Australia: II. A longitudinal study.

We conducted a longitudinal survey on 13 alpaca farms in four climatic zones of Australia to understand the epidemiology of gastrointestinal nematodes (GINs) of alpacas. A total of 1688 fresh faecal samples were collected from both sexes of alpacas from May 2015 to April 2016 and processed for faecal egg counts (FEC) and molecular identification of eggs using the multiplexed-tandem PCR assay. Based on egg morphology, the overall prevalence of GINs was 61% while that for strongyles was 53%. The overall mean FEC was 168 eggs per gram (EPG) of faeces, with the highest count of 15,540 EPG. Weaners had the highest prevalence (73%) and mean FEC (295 EPG) of GINs followed by tuis, crias and adults. Alpacas in the winter rainfall zone had the highest prevalence (68%) as well as FEC (266 EPG) followed by Mediterranean-type, non-seasonal and summer rainfall zones. Trichostrongylus spp. (83%, 89/107), Haemonchus spp. (71%, 76/107) and Camelostrongylus mentulatus (63%, 67/107) were the three most common GINs of alpacas across all climatic zones. The mixed-effects zero-inflated negative binomial regression model used in this study showed that it could help to design parasite control interventions targeted at both the herd level and the individual alpaca level. The findings of this study showed that the epidemiology of GINs of alpacas is very similar to those of cattle and sheep, and careful attention should be paid when designing control strategies for domestic ruminants co-grazing with alpacas.

Epidemiology of gastrointestinal nematodes of alpacas in Australia: I. A cross-sectional study.

This study involved a national cross-sectional survey of gastrointestinal nematodes (GINs) of alpacas in Australia. A total of 1545 fresh faecal samples were collected from both sexes of alpacas and processed for faecal egg counts (FEC) and molecular identification of nematodes using the multiplexed tandem PCR assay. Based on egg morphology, the overall prevalence of GINs was 66% while that for strongyles was 59%. The overall mean FEC was 276 eggs per gram (EPG) of faeces, with the highest count of 17,415 EPG. Male alpacas had a higher prevalence (68%, 334/490) as well as mean FEC (328 ± 60 EPG) of GINs than females (63%, 602/954; 227 ± 26, respectively). Weaners had the highest prevalence (80%) whereas tuis had the highest FEC (402 EPG) of nematodes. The highest prevalence (77%, 293/383) and FEC (630 EPG) of GINs were observed in the summer rainfall zone followed by the Mediterranean-type rainfall, non-seasonal rainfall and winter rainfall zones. The characterisation of nematode DNA isolated from faeces revealed the occurrence of seven different GINs, including Camelostrongylus mentulatus, Cooperia spp., Haemonchus spp., Oesophagostomum spp., Ostertagia ostertagi, Teladorsagia circumcincta and Trichostrongylus spp. Besides, Nematodirus spp. and Trichuris spp. were also found during FECs. The prevalence of Haemonchus spp. was highest in the summer rainfall zone while that of C. mentulatus was highest in the Mediterranean-type rainfall, non-seasonal rainfall and winter rainfall zones. The findings of this study revealed that alpacas harbour many of the same nematodes as sheep and cattle.