AUSTRALIAN HORSE DISEASE

To: virology@net.bio.net
From: Morley@admin3.usask.ca (Paul Morley)
Subject: Re: horse disease in Australia
Date: Thu, 8 Dec 1994 09:28:37

This was thought to be caused by a 
morbillivirus.  I have attached a posting from the chief veterinary officer of 
Australia to the OIE.  

Paul Morley
Morley@admin3.usask.ca
Western College of Veterinary Medicine, University of Saskatchewan, Canada

Dr Jean Blancou
Director General
Office International des Epizooties
PARIS
Dear Dr Blancou

Acute Equine Respiratory Syndrome in Brisbane, Queensland

The condition has been restricted to properties directly associated with 1 stable in the suburb of Hendra in Brisbane The situation as of 12 October 1994 is summarised in the following table:

Location     Descripti  No. of   No.      No. in-  Tot
             on         horses   dead or  contact  al
                        recover  euthana   Healthy
                        ed       sed
* Hendra 1   IP1        4        11       9        24
(Brisbane)
* Hendra 2   neighbour  1        1         10      12
(Brisbane)   to IP1
* Hendra 3   neighbour  0        0         7       7
(Brisbane)   to IP1
Cannon Hill  holding    0        1         14      15
(Brisbane)   associate
             d with
             IP1
Kenilworth   holding    1        1        300      302
(150 kms     associate
north of     d with
Brisbane)    IP1
Samford      holding    1        0        20       21
             associate
             d with
             IP1

Although there are 300 horses on this holding, the 2 affected horses from IP1 have not been in-contact with the other horses on this spelling property.

All negative to Serum Neutralisation test

The 7 recovered horses are positive on SNT

Extensive investigations have been undertaken by government veterinary authorities and private veterinary experts and known endemic and exotic diseases of horses have been excluded.

Clinical Signs

Of the 21 cases known to date, 14 have presented as an acute respiratory syndrome with death in 1 to 3 days. A further 4 animals have been clinically affected but recovered, while 3 have been virtually inapparent infections. Clinical cases have been inappetant and pyrexic (up to 410C) with shallow respiration and most having a frothy nasal discharge varying from clear to blood tinged. Mucous membranes have usually been dark to cyanotic and sometimes slightly jaundiced. Several animals were reported to have dependent oedema (angle of jaw, legs, sheath), ataxia and head pressing. Terminal animals have usually died in extremis with a copious frothy nasal discharge.

Pathology

The common feature at gross necropsy has been severe lung congestion and oedema with blood-stained stable froth in the airways. Other findings have been petechial and ecchymotic haemorrhages in various organs as well as slight jaundice. Microscopically, lesions are those of an acute interstitial pneumonia with damage to endothelial linings of small blood vessels, haemorrhage and foci of early necrosis.

Aetiology

The Australian Animal Health Laboratory (AAHL) and the Animal Research Institute, Queensland have isolated the same virus from 5 cases. Since the initial virus isolation, all further work with potentially infective material has been undertaken at AAHL. Studies at AAHL have shown this virus (AERS virus) belongs to the Paramyxoviridae family and may be a member of the Morbillivirus genus. Evidence for this includes:

• electron microscopy shows a nucleocapsid with a herring bone pattern typical of the Paramyxoviridae;
• AERS virus haemagglutinates guinea pig red cells but results are variable with red cells from other species;
• AERS virus does not possess neuraminidase which is consistent with the Morbillivirus genus;
• nucleotide sequencing studies suggest that the virus is a Morbillivirus but work is continuing in this area;
• immunofluorescent antibody studies on virus infected monolayers using antibodies to turkey rhinotracheitis, rinderpest, Newcastle disease, respiratory syncitial, mumps, measles, canine distemper, and parainfluenza 3 viruses were negative;
• immuno electron microscopy shows virus nucleocapsids to bind to labelled antibody to the isolated virus.
• Antibodies to parainfluenza types 1, 2 and 3 produce low level binding.

Transmission tests in 4 horses at AAHL have shown the isolated virus is the cause of the syndrome. Evidence for this includes:

• no bacterial pathogen or toxin could be detected; African horse sickness, equine influenza, equine herpes virus, equine viral arteritis and the equine viral encephalitides were eliminated;
• AERS virus was isolated from the lungs of 5 to 6 cases;
• specific antibody to AERS virus is present in 4 recovered cases and 3 in-contacts believed to have suffered a very mild and transient illness, but not in other horses;
• positive transmission tests to 4 horses, 2 of which received pure virus culture, with subsequent recovery of the virus at autopsy.

The incubation period in the natural cases was mostly 8 to 11 days with a maximum possible of 16 days. With the AAHL transmission tests, the incubation period was 3-12 days. Two suspect human cases had a putative incubation period of 5-8 days.

All the other cases (20) in horses and the suspect human cases can be linked to the original index case which was first observed sick on 7 September and died on 9 September.

From the pathogenesis, clinical picture and pattern of spread, natural transmission is most likely direct via frothy nasal discharges as a consequence of close contact or mechanical transfer. Aerosol transmission seems unlikely - the upper respiratory tract does not have lesions and coughing is not a feature of the syndrome.

Available evidence suggests that this virus is not highly contagious under conditions of natural transmission.

To date there is no evidence as to the possible source of the virus.

Serological Surveillance Results

AAHL has developed a Serum Neutralisation and an Immunofluorescence test and to date 1265 samples have been collected for testing. Results of 587 tests finalised to date, have shown that the only positive horses have been those located on, or originating from, the infected Hendra racing stable in suburban Brisbane. All horses within a 1 kilometre radius of this infected premises are being tested for presence of antibodies to this virus. Further results are expected within the next 48 hours. Blood samples have been submitted from areas outside the proclaimed Infected Area with all results to date being negative.

Movement Controls

Based upon surveillance results, the infected area has been reduced from a broad area of southeast Queensland to a 5 kilometre around the index premises and premises associated with direct movement of horses from the index stable. Limited horse race meetings have resumed in Brisbane and based on serological survey results indicating no seroconversion in horses not on quarantined premises all movement restrictions, except those applying to quarantine premises, have been lifted from midnight on 11 October 1994.

Public Health

The trainer of the horses also became affected with a severe respiratory condition and died on the 27 September 1994. The trainer, a stablehand, and the consulting veterinarian have seroconverted to the isolated virus. The stablehand exhibited influenza-like symptoms, but the veterinarian remained in normal health.

Blood samples from 18 other humans associated with this suburban location have remained sero-negative.

Transmission is believed to have been caused by very close contact with infected horses, for example hands in the mouth, and close contact with infected saliva.

The Queensland Director of Public Health has assured the general public that there is no public health risk from the equine virus.

I will keep you informed as further information becomes available.

Yours sincerely

GARDNER MURRAY

Australian Chief Veterinary Officer

Paul S. Morley
Department of Veterinary Internal Medicine
Western College of Veterinary Medicine
University of Saskatchewan
Saskatoon, Saskatchewan  S7N 0W0  CANADA
E-mail: Morley@Admin3.Usask.CA
Telephone: (306)966-7178
Fax: (306)966-7174