Lead Poisoning and Toxicokinetics in a Heifer and Fetus Treated with CaNa₂EDTA and Thiamine

Abstract

Abstract. Lead (Pb) poisoning of a pregnant heifer was diagnosed based upon clinical signs (head pressing, blindness, muscle twitching) and a blood lead concentration of 1.73 ppm. Blood and urinary Pb half-lives with CaNa 2 EDTA/thiamine therapy were determined to be 2.08 and 1.38 days, respectively. Many cations (Ca, Fe, Zn, Na, Cu), including Pb, were excreted at higher concentrations in urine during therapy. Blood (0.425 ppm) and liver (4.85 ppm) Pb concentrations in the fetus were 71.7% and 84.3% of the same tissue Pb concentrations of the dam, indicating a significant transfer of Pb in utero. Severe polioencephalomalacia was described in the adult, and hepatic lysosomes with metallic electron densities were present in the fetus.A severely depressed and dehydrated approximately 10-month-old angus heifer (175 kg, estimated) was presented to the Mississippi State University, College of Veterinary Medicine (CVM) Animal Health Center. The herd had recently experienced 2 acute yearling deaths due to unknown causes. This heifer had been found standing in a pond and was reluctant to move. Clinical signs included head pressing, staggering, muscle twitching, and lack of a menace response. Acute toxicosis (lead [Pb], organic pesticides, mercury) or a vitamin deficiency (vitamin A, thiamine) were suspected. Other rule outs included rabies, polioencephalomalacia, thromboembolic meningoencephalitis, listeriosis, and other less common central nervous system (CNS) differential diagnoses. 21 Blood was taken for a complete blood count (CBC) with differential, serum chemistry panel, and blood Pb concentration analysis. Initial therapy (day 0) consisted of thiamine hydrochloride a (1 g, intramuscular [im]), dexamethasone b (20 mg, intravenous [iv]), and oral electrolyte solution c (10 liters via stomach tube).The following morning the neurological signs were more pronounced and included, in addition to those previously noted, hyperesthesia, ptyalism, and bruxism. Blood Pb concentration was 1.73 ppm (CVM Diagnostic Services, Toxicology Laboratory, normal < 0.35 ppm) and the CBC and clinical chemistries were unremarkable. Day 1 treatments were 10 liters electrolyte solution per os, CaNa 2 EDTA d (13 g in 250 ml of saline iv), thiamine hydrochloride (1 g, im), and acepromazine maleate e (18 mg, im

Effects of calcium disodium EDTA and meso-2,3-dimercaptosuccinic acid on tissue concentrations of lead for use in treatment of calves with experimentally induced lead toxicosis

“…Analysis of results of the study reported here confirm those of other studies 3,5 in that they document that young, milk-fed calves are highly susceptible to lead toxicosis, as evidenced by the fact that within 10 days after initiation of oral administration of lead doses, all lead-treated calves developed several clinical signs compatible with lead intoxication. Furthermore, statistical analysis revealed that tissue lead concentrations of lead-exposed calves were significantly higher than those of control calves of group 1.…”

“…[1][2][3][4] Major clinical signs of lead toxicosis in cattle relate to the gastrointestinal tract or CNS and can include initial constipation followed by diarrhea (which may contain blood), abdominal pain, weak or abolished rumen motility, blindness, ataxia, dullness, lethargy, muscle fasciculations, and convulsions. 4,5 In other studies, [5][6][7] investigators have documented that extremely low doses of lead are capable of causing lead toxicosis in young milk-fed calves and susceptibility of such calves can be considerably affected by diets containing hay or grain.…”

Investigation of Heavy Metals in a Large Mortality Event in Caribou of Northern Alaska

“…Values were recorded as parts per million (ppm) wet weight (ww). Quality assurance and quality control were followed as in O'Hara et al (1995).…”

Retrospective study of cattle poisonings in California: recognition, diagnosis, and treatment

“…Histopathology of the brain will show evidence of polioencephalomalacia, such as cerebral laminar cortical necrosis, severe congestion of cerebrocortical tissue and meninges, edema, and endothelial swelling. 85,86 Severe liver necrosis and lipid accumulation, 81 and renal tubular degeneration, 82 may occur. Ante-mortem diagnosis of acute intoxication relies on history of exposure, clinical signs, and blood lead concentration greater than 0.35 µg/mL.…”

“…Ante-mortem diagnosis of acute intoxication relies on history of exposure, clinical signs, and blood lead concentration greater than 0.35 µg/mL. 85 It is critical to analyze a whole blood sample for lead. Serum and plasma samples are not appropriate for lead analysis because lead associated with red blood cells.…”