ARCHIVE FILE
This article was published in 1960
See the original document
INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Equine Infectious Anaemia
FIELD CLINICAL ASPECTS
OWEN H. BROOKS, B.V.Sc., Divisional Veterinary Officer, Rockhampton, Qld.
Introduction
Clinical pathological and serological investigations of a viral disease complex of horses in Central Queensland have been published in the Australian Veterinary Journal: Volume 35 April 1959 No. 4 p. 165-187. During the field investigations another viral infection, namely Influenza or "colds" has been considered as only six (6) positive transmissions have been recorded from the fourteen transmission tests from sick horses.
Since the publication of these papers, serum from field cases negative to E.I.A, has been examined by Dr. E. H. Doll (Lexington, Kentucky. U.S.A.), who found antibodies to Rhino-pneumonitis, which is considered to be the influenza virus.
This result is not surprising in view of the endemic nature of this disease until about 1910. It appears possible that the condition has not disappeared as some records suggest, but rather that it has remained relatively avirulent until recent years and has not aroused the attention of veterinarians; many of whom, including the writer, suspected its presence before E.I.A. was diagnosed.
DETECTION OF E.I.A.
E.I.A. may escape detection as it may effect only one horse in a group of from 20 to 200. Unless horses are subject to some stress to lower their resistance its presence may never be suspected. Under such circumstances an odd horse may be found dead; more especially brood mares and foals.
Under Central Queensland conditions the chief predisposing factor has been an excessive demand upon horses during Tick waves, when constant mustering under wet and bogey conditions becomes necessary.
In such circumstances, horses usually carry a heavy worm burden which adds to the stress factors during this critical period in station management. Because of the association of the appearance of symptoms with stress factors, this disease has probably escaped detection for a long period.
E.I.A. was first suspected in 1957 following a succession of "wet" years from 1950 to 1956, when Tick control became a real problem on the larger stations. Normally in Central Queensland there is only one good year in four. Then mustering for Tick presents a problem, but it is possible that in normal circumstances horses are not subject to the continued stress experienced during the phenomenal "wet" seasons from 1950 to 1956.
It is possible that the virus of E.I.A. became exalted in virulence on the affected properties during this period. Up to the present the heaviest losses of up to 25 have occurred on the larger stations carrying 200 or so horses where they are not treated individually as is the case on the smaller properties carrying from 20 to 40 horses.
The stockmen on the larger stations are usually indifferent about the care of horses and are not concerned with wastage or abuse. On the other hand, the horses on smaller properties usually are given more careful attention and are disposed in such a manner that they have an opportunity to recuperate on good pasture. On the larger stations horses generally are confined to one paddock; which predisposes to a heavy worm burden and a low plane of nutrition.
These factors may account for the higher incidence of cases of E.I.A. in Central Queensland (in contrast to the sporadic cases appearing elsewhere); though this is offered merely as a possible explanation. Smaller properties on the boundaries of the larger affected properties do not appear to have become involved, although odd deaths reported could have been due to E.I.A.
When E.I.A. appears on a property in a definite clinical manifestation, the following features usually are reported and observed:—
1. The general condition of the horse is below normal.
2. A heavy worm infestation often is suspected and may be present. However, affected horses do not improve following drenching.
3. Working horses show early fatigue.
4. Brood mares become emaciated and may die while rearing the foal.
5. Chronically affected horses continue to lose condition and become weak, anaemic and emaciated.
6. In the advanced stage of emaciation the blood is watery (Haemoglobin 3.5: R.B.C. 2 million: Cell to serum ratio 1:10).
7. In this condition dropsical swellings appear between the forelegs and on the sheath.
8. Odd horses may die suddenly in a tetanic spasm.
9. Horses are found dead in paddock
The problem confronting the veterinarian is the close similarity of clinical symptoms common to E.I.A. and Influenza (Rhino-pneumonitis); more specially when an individual horse is affected with acute symptoms common to both viral infections. These can be listed as follows:—
1. An acute, sub-acute and chronic febrile condition associated with depression, inappetence, nasal and ocular discharge.
2. Oedema of the eyelids, muzzle, belly, girth, sheath and legs.
3. Jaundice.
4. Purpura (usually follows an acute febrile reaction of up to 10 days).
5. Scouring (usually foetid).
6. Ataxia and weakness (some cases remain permanent).
7. Prostration, paralysis, tetanic spasms.
8. Albuminuria (Polyuria).
9. Deaths may be sudden following onset of symptoms.
10. Generalised pustular dermatitis and sloughing of skin is not uncommon.
11. Reports of abortions in mares are received.
DIFFERENTIAL DIAGNOSIS OF E.I.A. AND INFLUENZA
An outbreak of influenza is usually sporadic and may appear spontaneously over a wide area. It often follows horses returning from shows and rodeos.
A high incidence is common when working horses cannot be used for a period of approximately 3 weeks. If rested there is an uneventful recovery. Some horses, more especially thoroughbreds, may retain a cough for several months. If horses are worked when they have influenza the recovery may be slow during which the animal may become "poor" and show evidence of ataxia. Foals appear to be more susceptible and deaths following paralysis are not uncommon.
The virus of influenza appears to be haemotropic and a rapid loss of erythrocytes does occur, with a rapid sedimentation rate.
AIDS TO DIAGNOSIS
A blood sample from an advanced case of E.I.A. Usually gives a fair indication of the possible existence of the infection. The blood is watery, the sedimentation rate extremely rapid and the serum to cell ratio 1:10 (normal. 1:1).
On autopsy of the emaciated cases the liver usually is enlarged; showing a brownish deposit of haemosiderin. Several livers have weighed 28 lbs. (normal, 10-15 lbs.). In the more acute cases the spleen is enlarged and haemorrhages appear throughout the serous membranes. The lungs show a bright rust colour shortly after the cut surface is exposed to air. The kidneys usually are enlarged and fibrotic; with the serous surfaces jaundiced. The heart generally is enlarged and flabby; the muscle being extremely friable.
Laboratory diagnosis
A definite diagnosis of E.I.A. is dependent upon a febrile reaction and blood changes following the blood or serum inoculation of a susceptible horse under insectary conditions.
Owing to limited accommodation for horses, checking of field cases has been limited to those more likely to be E.I.A.