Proposed link between paralytic syndrome and thiamine deficiency in Swedish gulls not substantiated

Although Balk et al. (1) demonstrated decreased levels of thiamine in Swedish birds, the claim that thiamine deficiency causes the idiopathic neurologic syndrome seen is not substantiated by the evidence that these authors provide. The authors rely heavily on behavioral abnormalities in sick birds to corroborate their argument. However, many of the clinical signs described are shared by other diseases, including botulism and neurotropic viral infections. Postmortem examination and thorough diagnostic testing (apparently not done) are essential to rule out such etiologies. Furthermore, the authors present no evidence for lower tissue thiamine levels in paralyzed gulls compared with those not showing signs, an expected outcome in thiamine deficiency (2).

While citing a 2005 report concluding that the paralytic syndrome is not caused by any known pathogen (3) but which did not seek botulism, Balk et al. (1) largely ignored the 2004 investigation by Neimanis et al. (4) of gulls in the same area with similar clinical signs. After rigorous testing for numerous etiologies (although not thiamine deficiency), Neimanis et al. implicated type C botulism, with 69% of samples from affected birds in 2004 positive for toxin, no toxin in unaffected birds, and positive tests in gull samples dating back to 2000 (from the 2005 study, ref. 3). Detection of this potent biotoxin in serum from sick birds is diagnostic for botulism (5), but its detection in <100% of botulism cases is common in wild birds, including those experimentally intoxicated (6). Balk et al. (1) claim the paralytic syndrome differs from botulism in clinical presentation, but the signs and duration of botulinum intoxication vary among species. The hallmark is progressive, flaccid paralysis leading to respiratory difficulties (5), although not opisthotonus. Labored breathing is a sign of botulinum toxicity, based on experience with many species. Given the clinical signs and results of Neimanis et al. (4), botulism is a diagnosis that should have been excluded by Balk et al., by testing serum or treatment with antitoxin.

The authors claim as prima facie evidence for thiamine deficiency the improvement observed upon thiamine treatment of nine of 14 (not nine of 10; four treated birds were dropped from analysis) affected herring gulls collected over a 4-year period compared with six that received saline. However, thiamine has therapeutic benefits besides reversing a deficiency. At high doses, thiamine has a cholino-mimetic effect and can reduce the effects of other anticholinergic agents (7). Because botulinum toxin blocks acetylcholine release from nerve cells, thiamine injections might ameliorate botulinum intoxication, especially after ingestion of sublethal doses from which birds can recover, given rest, shade, water and feed. Contrary to the assertion made (ref. 1 and Table S3 therein), thiamine has reportedly improved survival of botulinum-inoculated mice (8) and has been used therapeutically in humans with food-borne botulism (9).

That thiamine levels are low in birds from southern Sweden is not disputed, and these low levels may contribute or predispose birds to other problems, including the paralytic syndrome. However, a more rigorous and multidisciplinary investigation is needed to discern the relative importance of the potential causes of this syndrome before the sweeping conclusions made by Balk et al. (1) can be accepted.