Coturnism

Coturnism is an illness featuring muscle tenderness and rhabdomyolysis[1] (muscle cell breakdown) after consuming quail (usually common quail, Coturnix coturnix,[2] from which the name derives) that have fed on poisonous plants.

Coturnism
Coturnix coturnix
SpecialtyToxicology

Causes

From case histories it is known that the toxin is stable as four-month-old pickled quail have been poisonous. Humans vary in their susceptibility; only one in four people who consumed quail soup containing the toxin fell ill.[3] The toxin is apparently fat-soluble as potatoes fried in quail fat have proved poisonous.[3]

Coniine from hemlock consumed by quail has been suggested as the cause,[4] though quail resist eating hemlock.[3] Hellebore has also been suggested as the source of the toxin.[5] It has also been asserted that this evidence points to the seeds of the annual woundwort (Stachys annua) being the causal agent.[3] It has been suggested that Galeopsis ladanum seeds are not responsible.[6]

Epidemiology

Migration routes and season may affect quail risk.[7] Quail are never poisonous outside the migration season nor are the vast majority poisonous while migrating.[3] European common quail migrate along three different flyways each with different poisoning characteristics, at least in 20th century records. The western flyway across Algeria to France is associated with poisonings only on the spring migration and not on the autumn return. The eastern flyway, which funnels down the Nile Valley is the reverse. Poisonings were only reported in the autumn migration before the quail had crossed the Mediterranean. The central flyway across Italy had no associated poisonings.[3]

Migrating quail used to be caught and eaten in prodigious numbers (150,000 quail exported from Capri in 1850)[8] but modern farming and droughts in the Sahel have led to a vast reduction in the size of the migrations. Conservation efforts and the availability of farmed quail have also reduced the consumption of these wild birds. Coturnism may well disappear before it is understood.

History

The condition was certainly known by the 4th century BC to ancient Greek, and subsequently Roman, naturalists, physicians and theologians. The Bible (Numbers 11:31-34) mentions an incident where the Israelites became ill after having consumed large amounts of quail in Sinai.[9] Philo gives a more detailed version of the same Biblical story (The Special Laws: 4: 120-131). Early writers used quail as the standard example of an animal that could eat something poisonous to man without ill effects for themselves. Aristotle (On Plants 820:6-7), Philo (Geoponics: 14: 24), Lucretius (On the Nature of Things: 4: 639-640), Galen (De Temperamentis: 3:4) and Sextus Empiricus (Outlines of Pyrrhonism: 1: 57) all make this point.

Central to these ancient accounts is the thesis that quail became toxic to humans after consuming seeds from hellebore or henbane (Hyoscyamus niger). However Sextus Empiricus suggested that quail ate hemlock (Conium maculatum), an idea revived in the 20th century. Confirmation that the ancients understood the problem, comes from a 10th-century text Geoponica, based on ancient sources. This states, "Quails may graze hellebore putting those who afterwards eat them at risk of convulsions and vertigo....".[10]

gollark: No.
gollark: Okay then.
gollark: Oh, well, you have 6 hours.
gollark: Also, you ARE to have your code guessing entry submitted.
gollark: It's a computer science lesson with Mr Wilde, however, that it would replace.

References
  1. Korkmaz I, Kukul Güven FM, Eren SH, Dogan Z (October 2008). "Quail Consumption Can Be Harmful". J Emerg Med. 41 (5): 499–502. doi:10.1016/j.jemermed.2008.03.045. PMID 18963719.
  2. Tsironi M, Andriopoulos P, Xamodraka E, et al. (August 2004). "The patient with rhabdomyolysis: have you considered quail poisoning?". CMAJ. 171 (4): 325–6. doi:10.1503/cmaj.1031256. PMC 509041. PMID 15313988.
  3. Lewis DC, Metallinos-Katzaras E, Grivetti LE (1987). "Coturnism: Human Poisoning by European Migratory Quail". Journal of Cultural Geography. 7 (2): 51–65. doi:10.1080/08873638709478507.
  4. Clatworthy, Menna (2010). Nephrology: Clinical Cases Uncovered. John Wiley and Sons. p. 145. ISBN 978-1-4051-8990-3.
  5. Dobbs, Michael R. (2009). Clinical neurotoxicology: syndromes, substances, environments. Elsevier Health Sciences. p. 166. ISBN 978-0-323-05260-3.
  6. Uriarte-Pueyo I, Goicoechea M, Gil AG, López de Cerain A, López de Munain A, Calvo MI (November 2009). "Negative evidence for stachydrine or Galeopsis ladanum L. seeds as the causal agents of coturnism after quail meat ingestion". J. Agric. Food Chem. 57 (22): 11055–9. doi:10.1021/jf902764n. PMID 19860419.
  7. Giannopoulos D, Voulioti S, Skarpelos A, Arvanitis A, Chalkiopoulou C (2006). "Quail poisoning in a child". Rural Remote Health. 6 (2): 564. PMID 16700632.
  8. Toschi A (1959). La quaglia: vita, caccia, allevamento. Supplemento alle Ricerche di Zoologia Applicata alla Caccia. 3. Bologna: Università di Bologna. p. 110. OCLC 66552512.
  9. Ouzounellis T (16 February 1970). "Some notes on quail poisoning". JAMA. 211 (7): 1186–7. doi:10.1001/jama.1970.03170070056017. PMID 4904256.
  10. Andrew Dalby Totnes (2011). Geoponica : farm work: a modern translation of the Roman and Byzantine farming handbook. Prospect. p. 294. ISBN 978-1-903018-69-9.
Classification
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