CASE NOTES


LEAD POISONING IN YEARLING CATTLE

Libby Read — District Veterinarian, North West LHPA

Posted Flock & Herd December 2011

INTRODUCTION

Four heifers died from a mixed mob of 45 yearlings grazing a sparse, mature oats crop on sandy soil near Pilliga, NSW. A necropsy of the fourth heifer to die revealed a substance of similar appearance to lead in the rumen and lead toxicity was confirmed via laboratory analysis of kidney tissue. Following confirmation of lead toxicity, the remaining yearlings were subject to regulatory restrictions on account of potential lead residues.

HISTORY

Forty five Hereford and Hereford cross yearling heifers and steers were grazing an oats crop intermittently during winter and spring of 2011. The paddock also contained areas of native pasture.

Figure 1: Yearlings on sparse oat crop

Two heifers were found dead by a neighbour in October 2011. The neighbour was checking the cattle occasionally as the owner was on holidays. Although the deaths were reported to the local District Veterinarian, an investigation was not undertaken due to the autolysed nature of the carcases. It was thought that facial eczema may have been involved due to grazing oats and prevailing damp environmental conditions. The District Veterinarian advised temporary removal of the cattle from the paddock. The yearlings were removed, but returned to the paddock when the owner returned a week later.

A third heifer was found dead on November 6th, but was not reported by the owner.

A fourth heifer was found dead at lunchtime on November 10th. The owner had observed the heifer in the 36 hours prior to death and she had appeared healthy.

The yearlings were not vaccinated with 5 in 1 clostridial. The owner reported that they were chewing on 'anything they can find' - wood, bags etc. A commercial lick was on offer, but the yearlings were not consuming it readily.

EXAMINATION AND NECROPSY

The heifer had died in sternal recumbency in the 'middle' of the paddock. Blood was oozing from the nose and conjunctivae were swollen and congested with blood. There were no signs of struggle. Other yearlings grazing the paddock appeared normal.

Figure 2: Dead heifer in situ

An Anthrax ICT test was conducted, with a negative result.

At necropsy the carcase was found to be autolysed (exacerbated by hot and humid weather conditions). The lungs, especially cranio-ventral lobes, were extremely congested with blood. The pericardial sac was full of blood. There were petechial haemorrhages on the epicardium but the myocardium appeared pale. The liver had rounded edges and appeared about 20% larger than normal. The kidneys were autolysed. The spleen appeared normal. There was a mixture of vegetation, barley grain (apparently the heifer was seen eating some barley spillage 48 hrs earlier) and a 'gravel-like' substance, possibly lead, in the rumen. There was barley and vegetation in the reticulum, omasum and abomasum. The lead-like substance was not found in the reticulum. The brain appeared grossly normal.

Figure 3: Congested thoracic tissues.
Figure 4: Lead fragments found in the rumen

Samples were sent for laboratory examination, with lead toxicity considered the most likely differential. Other differentials included lactic acidosis and acute septicaemia (possibly clostridial, or histophilosis).

The owner was advised to remove the yearlings from the paddock pending laboratory results and asked to look for a potential source of lead. The next day the owner advised that he had found evidence of a 'lead oxide' substance in ash where a pile of rubbish had been burnt in the paddock. He presumed that a car battery had been in the fire.

LABORATORY RESULTS

Comments: Kidney lead levels indicate toxicity

DISCUSSION

Lead is a common cause of poisoning in domestic animals (Seawright, 1989). Young cattle are often affected, presumably due to their inquisitive nature, with lead acid batteries being a common source (Radostits et al, 2007).

Cattle affected by lead may show signs within 2 to 3 days of ingestion, with neurological signs being commonly seen (Seawright, 1989). Death may occur within a few hours of onset of clinical signs, or up to several days later (Seawright, 1989). In acute cases, there is a sudden onset of clinical signs and death. Consequently many animals are found dead without any signs being observed (Radostits et al, 2007).

In most acute cases there are no gross lesions at necropsy.

Findings may include abomasitis, enteritis, epicardial haemorrhages, diffuse congestion of the lungs and degeneration of the liver and kidney (Radostits et al, 2007). In this case, the congestion of the lungs and pericardial fluid with blood was spectacular.

To confirm a diagnosis of lead toxicity post mortem, analysis of lead levels in the kidney or liver are preferred. A lead content of 260umol/kg wet weight in the kidney of this animal confirmed the diagnosis.

Stock exposed to abnormal lead intake must not be slaughtered for human consumption (Byrne and Gill, 2011). As such, this herd is subject to regulatory restrictions until animal health authorities are confident that their tissues meet food standards.

REFERENCES

  1. Byrne D and Gill P. Lead poisoning in livestock NSW DPI Primefact 413, 2011
  2. Radostits OM, Gay CC, Hinchcliff KW and Constable PD. Veterinary Medicine - A textbook of the diseases of cattle, horses, sheep, pigs and goats. 10th Edition. 2007. Saunders publishing. Pages 1799 - 1808
  3. Seawright AA. Animal Health in Australia, Volume 2 (Second Edition), Chemical and Plant Poisons. 1989. Australian Government Publishing Service, Canberra. Pages 211 - 215

 


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