CASE NOTES
The 2000 Akabane epidemic in the Narrabri district and lack of an Akabane epidemic in 2024 despite high monitoring herd seroconversions
Shaun Slattery, Local Land Services, Narrabri
Posted Flock and Herd August 2025
This paper outlines the features of the 2000 Akabane epidemic in the Narrabri Rural Lands Protection Board (RLPB) district, including results from a local National Arbovirus Monitoring Programme (NAMP) sentinel herd. It then compares this epidemic with similar high Akabane seroconversions for the 2023-24 season, but with an absence of reported clinical Akabane cases in the equivalent district for 2024. It presents serological evidence for the association of non-Akabane Simbu serogroup seroconversion in preceding years as protective against clinical Akabane epidemics.
Epidemics of epizootic bovine congenital arthrogryposis and hydranencephaly (AG/HE) syndromes in calves have occurred in NSW at irregular intervals since the mid-1940s1,2, with similar epidemics in Israel and Japan. In 1956, Blood2 described the condition and suggested an association between high rainfall summers and epidemics in the following year—that is, the possibility of the condition being caused by an arbovirus.
In 1975, Hartley et al.3 presented serological evidence for the association of Akabane virus with AG/HE syndromes in NSW. The following year, Della-Porta et al.4 reported results from a nationwide survey of 4,000 sera, which demonstrated the association between the extent of the 1974 AG/HE epidemic and seroconversion to Akabane virus. They also observed a correlation between Akabane antibody in cattle and the distribution of Culicoides brevitarsis. They proposed that AG/HE epidemics are caused by Akabane virus moving from an endemic situation into susceptible cattle populations as the distribution of the vector changes.
The National Arbovirus Monitoring Programme (NAMP) was established in 1992 to monitor the distribution of Akabane virus, Bluetongue virus, and Bovine ephemeral fever virus5. In 1995, monitoring of a NAMP sentinel herd within the Narrabri RLPB district at Pilliga commenced, with sampling in spring (usually October), mid-summer (January), autumn (April) and at the end of the season in winter (June/July). From 1995 to 2000, there were no Akabane seroconversions in the Pilliga NAMP herd.
Prior to 2000, clinical Akabane cases had not been diagnosed in the Narrabri RLPB, including during the 1974 major epidemic (JA Macfarlane, personal communication, 2000). In 2000, the author was the District Veterinarian for the Narrabri RLPB. The first warning signs of a possible Akabane epidemic came from export embryo testing near Narrabri. Five cattle sampled on 5 May 2000 were all seropositive for Akabane, having been negative when sampled on 22 March 2000.
Subsequently, calves with Akabane congenital defects were either confirmed by serology or strongly suspected based on clinical signs on 42 holdings in the Narrabri RLPB district. Anecdotally, almost all cattle herds in the district had affected calves, with reporting decreasing once the cause of the condition became widely known.
Despite the period of viral infection being short, major epidemics occur over several months, as the lesions are related to the stage of gestation when infection occurs1. The 2000 Narrabri epidemic followed the classic sequence described by Beveridge1.
The first cases were seen at the end of June with stillbirths of deformed calves. From early July, cases presented as dystocia/stillborn/polioencephalomyelitis (PE). The PE calves often could not rise and were easily confused with stillbirths as they were found dead where calved.
Arthrogryposis (AG) cases also started to present in early July and were soon the predominant syndrome. Classically, these calves had a single limb with fixed flexion.
From September to December, hydranencephaly (HE) or 'dummy calves' predominated. These showed varying severity of clinical signs, ranging from those unable to suckle to those able to feed but eventually dying due to misadventure. Few, if any, were both saleable and fit for transport to saleyards or abattoirs without compromising welfare.
Using gestation timelines and lesion patterns from Beveridge1, the infection period was estimated as late February to early May.
The Pilliga NAMP herd seroconverted to Akabane relatively late, with 1/10 in January 2000, no further seroconversions in April 2000, and 5/10 by June 2000.
Since 2000, only a single clinical case of Akabane has been diagnosed (in 2004), and Akabane seroconversion in the Pilliga NAMP herd has been rare and low prevalence. The Pilliga NAMP herd later moved to a similar holding 5 km south-west of the previous location.
Following the 2000 epidemic, additional NAMP herds were added in north-west NSW at Bellata and Boggabri, adjacent to the former Narrabri RLPB district boundaries.
In April 2024, Akabane seroconversion was observed in 3/15 animals at Pilliga. By July, this seroconversion rate had increased to 7/14. Bellata (5 km from the old Narrabri RLPB district boundary) showed 6/9 seroconversions in February. Boggabri (30 km south-west) had 1/14 seroconversions in February, 3/15 in April, and 4/15 by June. Additionally, clinical Bluetongue was diagnosed on three holdings in the autumn, indicating widespread Culicoides brevitarsis presence.
In response, North West Local Land Services (LLS) issued general awareness alerts to private veterinary practitioners (PVPs), including presentations at local Australian Veterinary Association meetings.
Despite increased awareness by District Veterinarians and PVPs, Akabane was only diagnosed on a single holding, where 10 of 70 cows had calves with classical HE signs over 2-3 weeks of an eight-week joining period. Diagnosis was confirmed by serology. Neighbouring properties regularly consulted with both PVPs and District Veterinarians and reported no suspect cases.
Thus, despite NAMP monitoring indicating extensive movement of Akabane virus into susceptible cattle, a clinical epidemic did not occur.
One possible explanation for this low level of clinical disease is the protective role of other viruses in the Simbu serogroup (DS Finlaison, personal communication, 2025). A review of prior NAMP Simbu serology supports this hypothesis. Laboratory data for the monitoring seasons preceding both the 2000 and 2024 seasons were sourced from the Livestock Health Monitoring System (LHMS), used by LLS District Veterinarians.
At Pilliga, Simbu seroconversion was negligible prior to 2000, with only 2/10 conversions in winter 1997. In contrast, as shown in Table 1, half of the animals seroconverted in each of the two years prior to 2024. The Boggabri herd showed even higher rates of Simbu seroconversion. This surge in non-Akabane Simbu seroconversion only occurred for two years, with negligible Simbu activity between 2021 and 2015.
Table 1. Winter sampling Simbu and Akabane seroconversions for Pilliga and Boggabri NAMP herds
(Pos = Positive; Samp = Sampled; Inconcl = Inconclusive)
| Year | Pilliga Simbu (pos/samp) | Pilliga Akabane (pos/samp) | Boggabri Simbu (pos/samp) | Boggabri Akabane (pos/samp) |
|---|---|---|---|---|
| 2023 | 7/15 (3 inconcl.) | 0/15 | 12/15 | 0/15 |
| 2022 | 8/12 | 0/12 (1 inconcl.) | 10/15 | 1/15 (1 inconcl.) |
| 2021 | 0/12 | 0/12 | 0/15 | 0/15 |
| 2020 | 0/12 | 0/12 | 0/15 | 0/15 |
| 2019 | 1/15 | 1/15 | 0/15 | 0/15 |
| 2018 | 1/15 | 0/15 | 2/15 | 1/15 |
| 2017 | 0/15 | 0/15 | 0/15 | 0/15 |
| 2016 | 0/15 | 0/15 | 0/15 | 0/15 |
| 2015 | 0/15 | 0/15 | 0/15 | 0/15 |
This paper describes a classical Akabane epidemic, typical of those that occurred sporadically in NSW from the 1940s until the early 2000s. It demonstrates that extensive Akabane virus activity in 2024 did not result in a clinical epidemic. A potential association between prior non-Akabane Simbu seroconversion and the absence of clinical cases is proposed.
Notably, at the state level, no widespread epidemics have been reported since 2003 (DS Finlaison, personal communication, 2025). This finding may reflect changes in the epidemiology of non-Akabane Simbu viruses and their influence on Akabane disease outcomes.
However, the evidence presented in this paper is associative rather than causative, and other possible explanations for the changes in the epidemiology of Akabane epidemics should be considered, including a reduction in virus virulence or changes in vector dynamics.
Acknowledgements
My District Veterinarian colleagues Judy Ellem and Justine McNally for provision of details on their NAMP herds, and Deborah Finlaison from the EMAI Virology Laboratory for insights into the relevant arboviruses.
References
- Beveridge WIB (1986) Animal health in Australia Vol. 1: Viral diseases of livestock. 2nd ed. Canberra: Australian Government Publishing Service; 1986 pp 3-10
- Blood DC (1956) Arthrogryposis and hydranencephaly in newborn calves: incidence and clinical findings Australian Veterinary Journal 32:125-31
- Hartley WJ, Wanner RA, Della-Porta AJ & Snowdon WA (1975) Serological evidence for the association of Akabane virus with epizootic bovine congenital arthrogryposis and hydranencephaly syndromes in New South Wales Australian Veterinary Journal 51(2):49-50 doi.org
- Della-Porta AJ, Murray MD & Cybinski DH (1976) Congenital bovine epizootic arthrogryposis and hydranencephaly in Australia: distribution of antibodies to Akabane virus in Australian cattle after the 1974 epizootic Australian Veterinary Journal 52(11):496-501 doi.org
- Animal Health Australia (2023) National Arbovirus Monitoring Program (NAMP): overview and history. Canberra: Animal Health Australia; 2023 [cited 2025 Apr 18] www.animalhealthaustralia.com.au