Quail poisoning is known to produce an acute myoglobinuric syndrome. T
he cause of this syndrome is still unknown. It has been suggested that
a toxic effect or a genetic sensitivity plays a major role. Ten patie
nts with a history of quail poisoning were examined to determine their
present state and the course of the disease. A muscle biopsy was perf
ormed in 2 of these patients who complained of muscle cramps after exe
rcise. The activities of several glycolytic, mitochondrial and lipolyt
ic enzymes were estimated. In all 10 patients the physical examination
, electromyogram findings and conduction velocities were normal. Serum
levels of CK, aldolase and lactic acid were also within normal range.
In the 2 patients with cramps, all enzyme activities were normal in m
uscle tissue. Our findings possibly exclude a preexisting enzyme defec
t as a cause of myoglobinuria in quail poisoning. Considering that 4 o
f our patients continued the consumption of quails without further pro
blems, we suggest that the major factor contributing to quail poisonin
g must be toxic.