Henrik Sundberg

Wild birds of declining European species are dying from a thiamine deficiency syndrome.

Wild birds of several species are dying in large numbers from an idiopathic paralytic disease in the Baltic Sea area. Here, we demonstrate strong relationships between this disease, breeding failure, and thiamine (vitamin B1) deficiency in eggs, pulli, and full-grown individuals. Thiamine is essential for vertebrates, and its diphosphorylated form functions as a cofactor for several life sustaining enzymes, whereas the triphosphorylated form is necessary for the functioning of neuronal membranes. Paralyzed individuals were remedied by thiamine treatment. Moreover, thiamine deficiency and detrimental effects on thiamine-dependent enzymes were demonstrated in the yolk, liver, and brain. We propose that the mortality and breeding failure are part of a thiamine deficiency syndrome, which may have contributed significantly to declines in many bird populations during the last decades.

Reply to Rocke and Barker: The question is not whether birds are affected by thiamine deficiency or botulism, it is about the order of events

Contrary to the suggestion by Rocke and Barker (1), we do not want to exclude botulism as a part of the investigated wildlife disorder (2), because botulism may be secondary to the thiamine deficiency syndrome. This possibility and the investigations by Neimanis et al. (3) are discussed in Text S5 in our SI Appendix (2).

Biotoxicity testing and chemical analysis at a munitions dumping area in the Stockholm archipelago (Baltic Sea) revealed low toxicity and low concentrations of lipophilic pollutants

The potential toxicity of lipophilic pollutants in surficial sediment from a munitions dumping area in the Stockholm archipelago (Sweden, Baltic Sea) was investigated by nanoinjection of sediment extracts into newly fertilized rainbow trout (Oncorhynchus mykiss) eggs. Mortality and several types of abnormal development of the larvae were analyzed as measures of biotoxicity. Biochemical variables, such as ethoxyresorufin O-deethylase (EROD) and ethoxycoumarin O-deethylase (ECOD) induction and acetylcholine esterase (AChE) inhibition were analyzed as measures of sublethal toxicity. Chemical analysis of selected poly chlorinated biphenyls (PCBs) and polycyclic aromatic hydrocarbons (PAHs) in the sediments was also performed. Neither embryo mortality, larval mortality, nor deformities showed any increase in the sites of the dumping area compared to the neighboring sites. Neither were there any important differences between the sites in the dumping area and the neighboring sites for the variables length, haemorrhages, heart sac oedema or yolk sac oedema, vertebral deformities, or other morphological disorders. The response was low also for the sub-lethal biochemical variables EROD activity, ECOD activity and AChE activity. The conclusion was that no measurable lipophilic toxicants were released from the dumped munitions. It should be emphasized, though, that the lack of toxicity is shown only for this relatively small dumping area and that the results cannot be extrapolated to other (larger) dumping areas without reservations. The potency of the sediment extracts from the investigated area to induce EROD and ECOD activities, can be explained by a background level of pollution, illustrated by the presence of a number of PCBs and PAHs.