Farmer's cattle die after burnt out car in field causes lead poisoning

Other animals on the farm are now subject to movement restrictions to protect the food chain. Stock image.
Other animals on the farm are now subject to movement restrictions to protect the food chain. Stock image.
Ciaran Moran

Ciaran Moran

A farmer in Cork lost two cattle to lead poisoning after a car was burnt out in a field where they were grazing.

Other cattle in the grazing group continue to be monitored by Department of Agriculture staff due to possible exposure. The animals are also subject to movement restrictions to protect the food chain.

The second sudden death in the space of one week in a small group of weanlings prompted the submission of the second case to Cork Regional Veterinary Laboratory (RVL).

The animal was in good body condition and only extensive petechial haemorrhages in the cervical and thoracic thymus were observed.

Since this lesion may in some instances suggest lead poisoning, a thorough search of the animals stomach contents eventually revealed four tiny fragments of metal.

They were heated over a bunsen flame and melted very quickly indicating a low melting point and the possibility of lead.

Further information also revealed that a car was burnt out in the field, though it was removed from it three weeks before moving the weanlings onto the field.

Subsequent testing confirmed that the kidney and liver lead concentrations were indicated high exposure to lead.

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Cohort animals were subsequently blood tested and three of the animals had lead levels above the normal range.

Continuous monitoring of those animals is ongoing, along with movement restrictions to protect the food chain.

Ragwort poisoning cases

There were some cases of ragwort poisoning submitted to the RVLs during the months of July and August 2017.

In one case, a 14-month-old bullock was submitted to Limerick RVL with a history of poor thrift.

An autopsy revealed that the liver was pale, shrunken and firm. There was no evidence of parasitic tracts or biliary duct calcification.

Laboratory findings included Dictyocaulus viviparous larvae in a faecal sample and a notable trichostrongyle burden (1,200epg). Examination of the liver revealed widespread dissecting fibrosis, bile duct proliferation and marked megalocytosis.

These changes are consistent toxic hepatopathy (liver dysfunction) due to pyrrolizidine alkaloids, most likely from the consumption of ragwort.

Two further cases of ragwort poisoning were delivered to Sligo RVL.

The first case was in a six-year-old cow which had presented with neurological signs such as head pressing, licking and chewing, trembling, tenesmus and cardiac arrhythmia.

There was no response to treatment. In the second case, a two-year-old heifer was affected showing behavioural changes, staring eyes, frothing and aggression.

The liver appeared excessively firm on post-mortem examination.

 Both cases revealed typical ragwort associated poisoning changes on examination of the liver.

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