Over the last few years Hendra virus exclusions have become a regular occurrence for local private veterinarians and District Veterinarians working in the Mid Coast Livestock Health and Pest Authority. In the 2 years from 1 January 2009 to 31 December 2010 there have been 16 Hendra Virus exclusions in divisions A and B of the Mid Coast LHPA (the old Kempsey RLPB area). Common differential diagnoses for Hendra Virus include Crofton weed poisoning, avocado poisoning, chemical poisonings including ionphor, lead and fluroacetate, botulism and acute bacterial infections including anthrax. Other causes of respiratory and neurological disease include pneumonia, equine herpes virus (neurological strain), Murray Valley encephalitis, exotic viruses such as African horse sickness, equine influenza, West Nile Virus, acute septicaemias, snake bite envenomation and purpura haemorrhagica (Queensland Department of Employment, Economic Development and Innovation 2010) . The following paper reports a suspect Hendra case that occurred in June 2010 for which DV assistance was requested for a Hendra exclusion and subsequent confirmation of a diagnosis.
The case was first reported on the 2nd of June 2010 via a telephone call from a local private veterinarian, requesting assistance to exclude Hendra virus as a diagnosis in 3 of 7 horses on a private property. The three affected horses had developed clinical signs which included nasal discharge and ataxia.
The owner reported that one 27 year old stock horse mare had been off her feed for 24-36 hours, had a bilateral green/brown nasal discharge and seemed weak and ataxic. The second horse, a 14 year old Clydesdale cross, had been off her feed for approximately 12 hours, was pacing, had a nasal discharge and was drooling saliva. A third horse, a 17 year old pony mare had refused to eat that morning and was described as 'unwell'. The owner had taken rectal temperatures of the 3 sick horses and all were within the normal range. Four other horses and 1 goat on the property were showing no signs of illness. The owner reported that flying fox colonies do visit the property to feed in the fruit trees, but no colonies roost on the property. Stock on the property had recently been given access to a new cut of large round bale grass silage. Prior to this the stock had been eating large round bale Barley silage. The 3 affected horses had been ridden 3 days prior to development of clinical signs without a problem. The owner was advised to avoid contact with the horses until a visit had been conducted.
A visit was organised to exclude Hendra virus. An appropriate entry/exit site was established. Full PPE was worn by personnel involved in the examination of livestock as recommended by Queensland Department of Employment, Economic Development and Innovation. This included P2 face mask, goggles, disposable full length overalls, gloves and rubber boots (Figure 1).
The first horse examined (the 550 kg 27 year old stock horse) had a heart rate of 40 bpm, normal chest sounds, normal gut sounds, rectal temperature 38.5 degrees celcius. There was a small amount of green tinged, watery nasal discharge. The lower lip was drooping and the tongue was easily pulled from the horse's mouth and poorly retracted. The mare was reluctant to move, although would walk slowly when encouraged. Some general muscle fasciculations were noted in the shoulder muscles.
Samples collected for Hendra virus exclusion included nasal swabs in virus media, and blood into plain, lithium heparin, and EDTA vaccutainers. . Samples were collected from the 27 year old stock horse mare only.
The second horses examined (the 650kg 14 year old Clydesdale cross mare) was sternally recumbent, but cardinal signs were within normal limits. This mare also had markedly reduced tongue tone. This mare was able to stand with assistance and muscle fasciculations were noted in the shoulder muscles when the mare was standing.
A third horse (the 330kg 17 year old pony mare) had only slight reduction in lip and tongue tone.
All 3 horses were reported by the owner to have been dropping feed over the last 48-72 hours and had been fed the new round bale silage. Of the 4 other horses on the property, 1 mare was on agistment and not fed the silage, a miniature stallion which also was not fed the silage, and 2 aged geldings, both of which had access to the silage but rarely eat hay or silage.
A provisional diagnosis of Botulism was made based on history of changing feeds to a new bale of silage and clinical signs. The 3 affected animals were treated with Flunixin meglumine (1.1 mg/kg) and prophylactic procaine penicillin (12mg/kg) given the risk of aspiration pneumonia. A very poor prognosis was given for the 2 larger affected horses, with the pony having a guarded prognosis at best. The owners were advised to cease feeding the silage immediately. The silage was examined and some wet and mouldy areas were noted although no animal carcases were seen.
The ongoing treatment of the horses was discussed with the owner, with the possibility of referral to an equine hospital for intensive medical management. Sydney University were contacted for possible availability of Botulinum antitoxin, which while not commercially available in Australia is available through Sydney University.
Ongoing treatment was handed over to the referring private veterinarians, who visited the property later that day and administered oral fluids to the most severely affected animal. Euthanasia of the worst affected horses was also discussed with the owners.
The following day, just over 24 hours after the initial diagnosis the Clydesdale mare was euthansed after becoming recumbent and unable to rise.
The stock horse mare was euthansed 3 days after the initial visit.
The pony mare continued to show clinical signs including dysphagia, pytalism, weakness and muscle fasiculations. Referral for intensive medical management was not possible due to financial constraints and the owners elected to treat the mare at home. Intravenous fluids were administered intermittently over the next fortnight, and the owners attempted to feed the mare using a watery slurry of horse pellets. The mare lost considerable weight over the next fortnight and continued to have dysphagia over a 16 day period. The owners reported that the mare took almost 4 weeks to return to normal eating ability. During the recovery phase, as the mare began to eat more, she suffered 2 episodes of colic, which were treated conservatively with pain relief (flunixin meglumine 1.1mg/kg).
PCR performed on nasal swabs were reported negative for Hendra virus 2 days after the initial visit, with final results from AAHL including indirect ELISA, N and P gene TAqMan asssays reported negative 9 days after the initial visit.
Botulism is a disease characterised by progressive flaccid paralysis caused by the exotoxin produced by the obligate anaerobic, spore forming gram positive rod, Clostridium botulinum. On a weight basis the Clostridium botulinum neurotoxin is the most potent and lethal neurotoxin known to mankind (Johnson et al 2010). Botulism in horses can be categorised in 2 ways. The first is by the C botulinum serotype involved, and the second is by the route of acquisition. Horses may aquire the disease one of 3 ways, via the ingestion of preformed toxin (food borne), by ingestion of spores and germination and elaboration of toxin in the gastrointestinal tract (toxicoinfectious), or by the contamination of wounds and subsequent toxin elaboration. In foals the most common route is toxicoinfectious, whilst in adults food borne botulism is most common. It is suspected in this case that the round bale silage was the source of toxin, though no samples were submitted to identify or isolate botulinum toxin.