| Scott Fritz, DVM, ABVT Toxicologist Beef Cattle Institute Kansas State University Scottfritz@vet.k-state.edu |
Sources
Batteries, paint, older oils and greases, some solders, multiple others.
Mechanism
Lead has a variety of effects on different biochemical processes in the body. Generally, lead binds sulfhydryl groups deactivating some enzymes, lead competes with calcium ions replacing calcium in bone and altering conduction in nerves and muscle, lead also alters vitamin D metabolism and interferes with GABA activity in the CNS.
Signs
Clinical signs vary by species. In ruminants, acute lead exposures cause neurologic signs. Blindness is maybe the most recognizable and reasonably consistent sign. Other clinical signs include depression or hyperesthesia, ataxia, seizures, aggression, head pressing, muscle fasciculations, and death. Gastrointestinal signs including bloat and diarrhea may be appreciated.
Treatment
The classical antidote for lead poisoning in large animals is Ca-EDTA. Ca-EDTA can liberate lead from bone causing an increase in blood lead and worsening clinical signs. Chelation therapy in food animals is not recommended for multiple reasons including poor response to treatment, significant supportive care, and significant residue issues. In addition, there are no FDA-approved antidotes for food animals, thus, FARAD should be consulted prior to use. Regulations regarding lead exposure in food animals varies by state. The state veterinarian should be contacted, and some states will quarantine entire herds until blood lead concentrations drop below specified thresholds.
Diagnosis
Diagnosis is heavily dependent upon elevated concentrations of lead in the body. Ante-mortem testing is easily accomplished with whole blood. Postmortem sampling should include liver and kidney lead concentrations. Histologically, lead exposure can cause polioencephalomalacia, it is important to consider water deprivation/salt poisoning, and elevated dietary sulfur in clinical cases.
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