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This article was published in 1991
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Investigation of a Cattle Feedlot Mortality

SJ Whittaker BVSc, District Veterinarian, ALBURY/HOLBROOK

This report backgrounds the investigation of a cattle feedlot mortality that ultimately resulted in the death of 66 ex 200 cattle.

Particular attention is given to the attempts to establish the cause of the mortality. Consideration is also given to the problems encountered as a result of the unfortunate (though not illegal) movement of cattle ex the feedlot to other areas of the State and interstate and poses the question as to how similar incidents could be better managed in the future.

HISTORY

The feedlot was located on flat, though adequately drained land, on a State Forest lease at Yanco in the Riverina District of New South Wales. The owner had operated the feedlot for a number of years. At the time of the mortality approximately 200 steers and bulls (ranging from 18 to 30 months of age) had been on the lot for some 7 weeks with no significant prior health problems.

FEEDLOT RATION - was a particularly high roughage ration and contained:

132kg of clover hay

100kg of straw

120kg of Triticale

100kg of Wheat

50kg of Pollard

20kg of Pea Flour

5kg of Urea.

The ration was home mixed by the farmer in his own 'mix-all' unit. Clover hay was also fed ad lib.

A new batch of feed was prepared 2 days prior to the initial recognition of the problem and this ration was prepared by a different person than normally performed the task. At this most recent mixing granular urea which had been previously used was replaced by a powdered form of urea and this was added to the mix by volume and not by weight. The water supply wasad lib. from a tank filled from a local bore.

INITIAL PROPERTY VISIT (at which time 1 steer had just died and 12-15 appeared ill):

CLINICAL SIGNS (which were not uniform):

Affected animals stood apart from the mob and were reluctant to move; moved with a staggery gait (particularly swaying hindquarters); no obvious laminitis/ founder; anorexia; some with increased salivation ; no ocular discharges; some with diarrhoea; (green/brown in colour). No holding facilities of any form were available for closer inspection of clinical cases and as such temperatures were not recorded at this time.

POST-MORTEM FINDINGS (on the first deceased steer):

Rumen very full (atonic); no excessive grain obvious and no damage to ruminal mucosa; abomasum- mild inflammation, some ulceration; SI/LI- remarkably little content; liver- chronic fascioliasis; a few small haemorrhages on epicardium and splenic surfaces; some petechiation on the lungs; kidneys normal; no oral, buccal or ocular lesions.

DIFFERENTIAL DIAGNOSIS:

Urea poisoning;

Mycotoxicosis;

Lactic acidosis (considered unlikely due to the fact that this was a high roughage ration and no excessive grain had been noted in the rumen at autopsy);

Botulism;

Salmonellosis.

ACTION AT THIS STAGE:

Owner advised to remove the remainder of the feedlot ration and supplementary feed hay. A range of samples was forwarded to the laboratory.

DAY TWO OF INCIDENT:

A further 6 steers died overnight, further action-

The remainder of the feedlot ration was removed (the owner had not done so)

Hay was fed to the mob

15 sick steers were removed to an isolated area and one steer was shot for autopsy

Clinical findings were as previously mentioned.

SECOND AUTOPSY:

The autopsy was remarkable for its almost total absence of pathological findings- nil haemorrhages; all major organs appeared normal; rumen/SI/LI as with previous autopsy; no oral lesions; gall bladder enlarged.

FURTHER ACTION:

As the majority of cattle in the lot appeared healthy and were in near finished condition, the owner was advised to sell all healthy stock as soon as possible directly to the local abattoir.

As to the possibility of disposing of the 'remaining healthy' stock through fat sales, it was pointed out to the owner that as the problem was believed to be toxic and not infectious, quarantine would not be imposed. However it was made clear that we considered it morally wrong to dispose of the remaining stock other than direct to slaughter.

Unfortunately the owner was unable to arrange direct slaughter through the local abattoir and the following day 145 apparently healthy animals were forwarded to saleyards at Finley and Wagga. Again unfortunately 78 of these animals were purchased as stores and freighted to Singleton on the New South Wales North Coast. The majority of the remaining animals were purchased by meat buyers, but a small number were picked up by various other owners including some into Victoria.

Over the following week further deaths occurred amongst the remaining stock on the original feedlot; and deaths were also reported from the cattle forwarded to Singleton where 5 animals were found dead on arrival. Traceback information indicated that isolated deaths occurred on 2 other properties, one at Picola in Victoria.

A wide range of samples were collected by both private and Government veterinarians form a number of these cases and forwarded to various laboratories throughout the State for further examination. What follows is a summary of the principal findings of those investigations.

CLINICAL SIGNS:

As described earlier with the additional information that some affected animals had temperatures in the range 40-41.7 deg C.

GROSS PATHOLOGY:

Petechial haemorrhages of subcutaneous tissues; full rumen with reasonably dry content indicative of ruminal atony; rumen pH 6.7; slightly enlarged liver with rounded borders; inflamed and congested abomasal mucosa; lungs with some hepatisation and pneumonia (inhalation).

BACTERIOLOGY:

Pasteurella multocida was cultured from the initial case and from the lungs of a number of subsequent cases but the laboratory viewed this as most probably secondary infection.

BIOCHEMISTRY:

Abomasum and ruminal contents were tested for the presence of lead and arsenic with negative results.

VIROLOGY:

Submitted samples were virus isolation negative for Pestivirus and IBR.

URINALYSIS:

No significant findings.

HAEMATOLOGY:

A severe and pronounced leucocytopaenia was a uniform finding in all cases from which blood samples were submitted.

HISTOPATHOLOGY:

The major findings were confined to the liver, lymph nodes and red bone marrow. In summary these tissues indicated a hepatic paracentral necrosis, serous hepatitis, haemorrhagic diathesis, a deficit of red bone marrow and a necrotising lymphadenitis and a lack of immune response within the lymph node (to a generalised bacterial invasion of tissues).

TOXICOLOGY:

Both tissue and feed samples were forwarded for testing for organophosphate and organochlorine residues with negative results.

Feed samples were also forwarded to a number of laboratories for evaluation, particularly in relation to urea content. The urea levels were found to be within normal limits (less than 2% urea). Further feed samples were also forwarded to B.C.R.I. at Rydalmere for examination for fungi and mycotoxins. The clover hay produced only saprophytic fungi. The only toxin producing fungi were found in the cracked wheat and triticale samples (Aspergillus flavus) and this latter finding was discounted as the histopathology findings were not consistent with aflatoxacosis.

Feed analysis was negative for useful information.

FINAL OUTCOME OF THE INCIDENT:

A total of 66 cattle out of the original 200 head at the Yanco feedlot died. Deaths occurred over a period of 10 days with 47 dying at the feedlot, a further 16 deaths at Singleton plus 2 other isolated deaths.

While not all sick animals died, the overwhelming majority that developed clinical symptoms did. Antibiotics and various supportive and symptomatic treatments seeming to be of little benefit.

In an unfortunate sequel to the incident, legal proceedings for recovery of losses sustained were instituted against the owner of the feedlot by the party purchasing the stock that went to Singleton. The matter was settled out of court with undisclosed reparations being paid.

DISCUSSION:

At various stages of the investigation a wide range of aetiological possibilities were considered. These included:

* urea poisoning;

* mycotoxicosis;

* pesticide toxicity;

* haemorrhagic septicaemia (pasteurellosis);

* viral infection such as Pestivirus;

* exotic disease: the possibility of an exotic disease was ruled out at an early stage, findings were not characteristic of Rinderpest.

The majority of these possibilities were eliminated by a wide range of tests.

In summary the overall picture was one of haemorrhagic diathesis and leucocytopaenia.

Histopathological evidence favoured a diagnosis of mycotoxicosis but from a source unknown. The differential diagnosis of haemorrhagic diathesis/leucocytopaenia (radiomimetic syndrome) is listed in Blood, Radostits and Henderson (1983) as :

* Trichlorethylene extract of soya bean meal.

* Toluene.

* Trichothecine toxins, from Stacybotrytis or bracken fern.

* Radioactive material,

* Furazolidone poisoning.

Of these possibilities a trichthecine toxin would seem to have been the most likely. It would appear that some toxic elements (perhaps Stachybotrytis) caused death and suppression of cell lines in the bone marrow. The overall suppression of the immune system then allowed secondary bacteria to penetrate the animals' defence system and cause death.

In an interesting parallel to this case Jeffere and Lenghaus (1986) record the death of 22 Dairy Shorthorn cows and heifers over a 6 week period from suspected mycotoxicosis and in particular Stachybotrytoxicosis. In this case clinical signs observed in affected cattle included elevated temperature (41.4 deg C); ruminal atony; diarrhoea and rapid weight loss. Again intensive antibiotic treatment and blood transfusion did not ameliorate the clinical course, with cattle usually dying within 3-5 days after first appearing ill. Pathological findings again were consistent with a radiomimetic syndrome. In the weeks preceding overt disease, weather conditions were hot and humid and with abundant pasture litter, factors prevailed which favoured the proliferation of fungi (suspected of causing the condition on the pasture.

In the Yanco feedlot incident it appeared probable that some of the grain supplies had also become wet. Similar hot and humid weather conditions also prevailed during the time preceding the Victorian episode.

Stachobotrys chartarum is a fungus that multiplies and produces powerful toxins (trichothecenes) on hay, grain or pasture litter under restricted conditions of temperature and humidity. The trichothecenes in general are radiomimetic and affect rapidly dividing cells, such as those of the bone marrow, lymphoid tissue nodes and interdigital crypt epithelium.

Where the disease manifests as a general toxicosis, secondary bacterial infections play a major role in the course, clinical manifestation and outcome of the disease. This is ascribed to a marked immunosuppression involving both the cellular and humoral immune systems, a direct consequence of toxic action by the ingested toxins on leucocytes.

References:

Jeffers & Lenghaus (1986) Australian Veterinary Journal, 63: 263-264

Blood, Henderson & Radostits (1983) Veterinary Medicine, p 315


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