Abstract

A group of 5 bottlenose dolphins was diagnosed with an acute lead intoxication. The animals, 2 adult nursing females with their respective male calves, and a juvenile female, were kept within the same pool complex. The cases started with one of the nursing females (Animal 1) and the juvenile dolphin (Animal 2) showing sudden anorexia and signs of gastrointestinal discomfort with only 24 hours of difference. Blood samples were immediately collected for a full screening including CBC, serum chemistry, iron, fibrinogen, and a serum proteinogram. Due to the icteric color of the serum, lead poisoning was rapidly considered in the differential diagnosis. Thus, a determination of heavy metals in blood was requested to an external lab. The results of the CBC were unremarkable and the blood chemistry only showed some minor alterations in liver parameters and a decrease in the Alkaline Phosphatase. However, the heavy metals panel revealed a high concentration of lead in the samples: 1121 µg/L and 876 µg/L for Animal 1 and 2 respectively. The levels of lead in all animals of the same group were consequently evaluated with results ranging from 666 µg/L to 1726 µg/L. Immediate supportive treatment was implemented, and further diagnostics to determine the severity of the situation were performed. Lead pellets were observed in the first and second stomach chambers in the three females and in one of the calves. Some of these pellets were retrieved during a gastroscopy. One of the calves had no pellets but the highest concentration of lead in his blood. He was considered to have received the lead indirectly through his mother’s milk. Therapy consisted of vitamin B complex, folic acid, antacids, active carbon, liver protectors, analgesics, lead chelators (DMSA and EDTA), nutritional support and fluids. Eventually, corticoids, diuretics, sucralfate, prokinetics, paraffin oil, vitamin K and Yunnan Baiyao had to be included in the medical plan to treat the complications of the intoxication. Nursing females were milked 2–3 times a day to reduce the chances of poisoning the calves, and to somehow stimulate the elimination of lead through the milk. Though, the calves were not observed trying to nurse at any time since the poisoning started. The entire treatment required up to 5 maneuvers a day per animal while depending on the help of foreign suppliers and colleagues to have access to the chelators and enough supplies of certain components of the treatment. Despite the enormous efforts and the clear reduction in lead concentration in the blood resulting from the use of the chelators and the therapy, the three females died within the first month. Animal 1 showed severe normocytic normochromic anemia, mildly regenerative, and high count of NRBC (4%) before death. Histopathology of the bone marrow revealed a severe state of depletion of all stem cell lines, and a general adipose metaplasia in the three animals. At this point the calves seem to be thriving. The long term effects of the lead intoxication remain unclear and will need to be monitored.

Acknowledgements

The authors wish to thank Dr. Kerstin Ternes from Duisburg Zoo (Germany) for her immediate disposition to help with the logistics, and all the colleagues from the Veterinary Committee of the European Association for Aquatic Mammals for their unconditional support. Besides, we would like to highlight the incredible and enriching discussions shared with the Veterinary team of the National Marine Mammal Foundation, your knowledge and expertise made us all better and stronger. We also appreciated the support provided by the Veterinary staff of Sea World and Ocean Park in Hong Kong, and Dr. Paola Unda Marron. Finally, we would like to thank every single member of the staff at Mediterraneo Marine Park for their tireless energy and emotional strength in such a difficult period.