WA Livestock Disease Outlook - for vets

Livestock disease investigations protect our markets

Australia’s ability to sell livestock and livestock products depends on evidence from our surveillance systems that we are free of particular livestock diseases. The WA livestock disease outlook – for vets summarises recent significant disease investigations by Department of Primary Industries and Regional Development (DPIRD) vets and private vets that contribute to that surveillance evidence.

Catch up with local private and DPIRD vets at the DPIRD shed at Dowerin Machinery Field Days

Local private vets and the DPIRD Northam and Moora vets will be at the DPIRD shed at Dowerin Machinery Field Days this week to assist with any veterinary and biosecurity queries you may have.

Take the opportunity to drop in and pick up a handy summary factsheet of all the subsidies available for disease investigations that you can hand to clients, and to catch up on with your colleagues. There will also be other resources for your clients including factsheets on common sheep diseases, correct pig feed, pig biosecurity and on emergency diseases including foot-and-mouth disease and African swine fever.

Recent livestock disease cases in WA

Hendra virus excluded in two cases of neurological signs in horses

  • In June, there were two separate cases of neurological signs in horses in which Hendra virus was excluded.
  • In the first case, a 20-year-old pony had a one-week history of unilateral blindness, ataxia, reduced proprioception and circling. These signs progressively worsened, and the horse became pyrexic, lethargic, depressed and inappetent. The horse was not vaccinated for Hendra virus and there was no history of travel. There was one other horse on the property, as well as some sheep, none of which were displaying any clinical signs.
  • In the second case, a single horse agisted with 30 others displayed dullness, ataxia, dyspnoea, nasal discharge and anorexia. The horse also had an extended head and neck and bloody oral discharge. The horse was penned in an area where flying foxes were roosting. No other horses at the property were unwell, and the horse did not have a current Hendra virus vaccination.  
  • In both cases, a private vet examined the animals and considered the possibility that the clinical signs were due to a reportable disease such as Hendra virus. Given the zoonotic potential of this virus, it was imperative to avoid contact with the horses until exclusion testing was conducted. The private vets contacted DPIRD to arrange for laboratory testing, which was subsidised by DPIRD.
  • Fortunately, in both cases the horses tested negative for Hendra virus. Testing for other emergency diseases of horses was also negative, including equine influenza, equine encephalomyelitis, equine herpes viruses 1 and 4, West Nile virus, Murray Valley encephalitis and rabies.
  • In the first case, while reportable diseases were ruled out, a definitive diagnosis could not be established, and in the second case, a dental abscess was suspected as the cause of the clinical signs.
  • Hendra virus can be transmitted to horses by exposure to secretions from infected flying foxes, including their urine. A case has never been reported in horses in Western Australia, however flying foxes in northern WA have shown evidence of exposure to Hendra virus, presenting a risk to horses in contact.
  • The virus can be transmitted from infected horses to people, and it may cause serious, frequently fatal disease in humans. There have been four human deaths in Australia since the virus was first diagnosed in 1994, all occurring in Queensland.
  • For further information on Hendra virus, including how to reduce the risk of horses becoming infected, and safety advice for veterinarians, see the Hendra virus webpage

Private vet helps rule out foot-and-mouth disease (FMD) in calves in the South-West

  • In a herd of 150 two-month-old Angus cross calves, one had died and one was unwell showing severe pyrexia, nasal discharge and respiratory distress.  
  • A private vet performed a post-mortem on the one dead calf, and found froth in the trachea and lungs, and multifocal ulcerations around the larynx.
  • A full range of bloods, fresh and fixed tissues was submitted to the DPIRD laboratory, with the private vet suspecting infectious bovine rhinotracheitis or calf diphtheria (necrobacillosis).
  • Histopathology identified a severe ulcerative laryngitis with intralesional mixed bacteria, acute hepatocellular necrosis and diffuse pulmonary oedema.
  • The reportable diseases foot-and-mouth disease and vesicular stomatitis were excluded through testing on laryngeal tissue and bloods.
  • Bacterial culture of the laryngeal tissue isolated Bacteroides pyogenes, which is an opportunistic pathogen. The disease was attributed to a bacterial infection, possibly associated with a failure of passive transfer.
  • Reaching a diagnosis allowed the private vet to work with the producer to manage the disease.
  • Given that this investigation provided evidence of Australia’s freedom from trade-sensitive diseases, DPIRD paid the laboratory fees.
  • Clinical signs consistent with foot-and-mouth disease (such as shown in Figure 1) should always be reported to a DPIRD vet or the Emergency Animal Disease hotline on 1800 675 888. Early detection = faster eradication.
Drooling is a key sign of foot-and-mouth disease in cattle. Always call a vet if you see cattle drooling.
Figure 2: Drooling is a key sign of foot-and-mouth disease in cattle.

Neurological signs in Merino hoggets in the Wheatbelt

  • A DPIRD vet was contacted by a Wheatbelt producer about nervous signs in one-year-old Merino ewe hoggets. Of the flock of 200, one had died and other animals had been found separated from the group, obtunded, staring into space, with some appearing blind.
  • The DPIRD vet visited the property and conducted an on-farm investigation and a post-mortem on the dead ewe. It was in good body condition, with no significant gross pathological lesions. Fresh and fixed tissues and ocular fluid were submitted to the DPIRD laboratory with a provisional diagnosis of polioencephalomalacia (PEM).
  • Histopathological examination revealed chronic PEM of at least several days’ duration, characterised by extensive lamellar malacic lesions affecting the cerebral cortex. These findings correlated with the clinical history of several days of neurological impairment (see Figure 2).
  • The most common cause of PEM in WA is thiamine deficiency, which reduces energy availability to the brain and causes a classic pattern of degeneration. Most outbreaks of PEM are sporadic and affect only a couple of animals in a mob, but death rates of up to 10% have been reported.
  • Less common causes of PEM include lead toxicosis, sulphur toxicosis, salt poisoning, or consumption of certain plants including bracken fern, Nardoo fern and horsetail.
  • For more information on PEM, including treatment, see our PEM webpage.  
Relatively normal cerebral grey matter (bottom right) transitions to oedematous grey matter (top left) with infiltrating plump, round Gitter cells (phagocytic glial cells).
Figure 2: Relatively normal cerebral grey matter (bottom right) transitions to oedematous grey matter (top left) with infiltrating plump, round Gitter cells (phagocytic glial cells).

In late winter/spring, watch for these livestock diseases

Disease, typical history and signs

Key samples

Selenium deficiency in lambs and calves

  • Occurs in young animals as they have an increased demand for the essential trace element during growth and have not accumulated the reserves of adult animals.
  • Animals are typically grazing lush, rapidly growing pasture or legume-dominant pasture in the higher rainfall areas of the southwest coastal regions.
  • Paddocks heavily fertilised with sulphur-containing products or superphosphate applications may also predispose animals to deficiency.
  • Key signs: poor growth, stiff gait, arched back, apparent lameness, reluctance to move and sudden death.
  • Animals that show visible signs of deficiency can be supplemented in the short term with a selenium injection or drench. Care should be taken with dose rates and intervals as too much selenium can be fatal in stock.
  • Read more about selenium deficiency in sheep and cattle and how to prevent animals becoming deficient in the long term.


  • Blood in lithium heparin
  • Feed samples (total mixed ration)


  • Liver, fresh and fixed


  • Caused by the zoonotic bacteria Listeria monocytogenes. Sources of infection include contaminated soil or where asymptomatic animals (including rodents) have shed the bacteria in their faeces and in feed that is spoiled.
  • Primarily reported in winter and spring when heavy rainfall is more likely to spoil silage and cause a reduction in acidity that enhances the bacteria’s growth.
  • Livestock then consume contaminated feed material and can be infected via damage to the oral mucosa caused by rough feed. Silage should be properly prepared and inspected before feeding and leftover feed cleared away.
  • Key signs: neurological signs (due to encephalitis), recumbency and deaths. May cause abortions 5-6 weeks prior to lambing, stillbirths or newborn lamb deaths.


  • Cerebrospinal fluid


  • Fixed brain, fresh spinal cord and liver, brain stem swabs
  • If neurological signs are present, discuss with your DPIRD vet subsidies for TSE testing