The Chilopoda, or centipedes ([fig. 14]), unlike the millipedes, are predaceous forms, and possess well developed poison glands for killing their prey. These glands are at the base of the first pair of legs ([fig. 15]), which are bent forward so as to be used in holding their prey. The legs terminate in a powerful claw, at the tip of which is the outlet of the poison glands.
The poison is a limpid, homogeneous, slightly acid fluid, which precipitates in distilled water. Briot (1904) extracted it from the glands of Scolopendra morsitans, a species common in central France, and found that it was actively venomous for the ordinary experimental animals. A rabbit of two kilograms weight received an injection of three cubic centimeters in the vein of the ear and died in a minute. A white rat, weighing forty-eight grams, received one and a half cubic centimeters in the hind leg. There was an almost immediate paralysis of the leg and marked necrosis of the tissues.
As for the effect on man, there is little foundation for the fear with which centipedes are regarded. Our native species produce, at most, local symptoms,—sometimes severe local pain and swelling,—but there is no authentic record of fatal results. In the tropics, some of the species attain a large size, Scolopendra gigantea reaching a length of nearly a foot. These forms are justly feared, and there is good evidence that death sometimes, though rarely, results from their bite.
One of the most careful accounts of death from the sting of the scorpion is that of Linnell, (1914), which relates to a comparatively small Malayan species, unfortunately undetermined. The patient, a coolie, aged twenty, was admitted to a hospital after having been stung two days previously on the left heel. For cure, the other coolies had made him eat the head of the scorpion. On admission, the patient complained of "things creeping all over the body". Temp. 102.8°. On the fourth day he had paralysis of the legs, and on the fifth day motor paralysis to the umbilicus, sensation being unaltered. On the sixth day there was retention of the urine and on the ninth day (first test after third day) sugar was present. On the thirteenth day the patient became comatose, but could be roused to eat and drink. The temperature on the following day fell below 95° and the patient was still comatose. Death fifteenth day.
Examination of the spinal (lumbar) cord showed acute disseminated myelitis. In one part there was an acute destruction of the anterior horn and an infiltration of round cells. In another portion Clarke's column had been destroyed. The perivascular sheaths were crowded with small round cells and the meninges were congested. Some of the cells of the anterior horn were swollen and the nuclei eccentric; chromatolysis had occurred in many of them.
As for treatment, Castellani and Chalmers (1910), recommend bathing the part well with a solution of ammonia (one in five, or one in ten). After bathing, apply a dressing of the same alkali or, if there is much swelling and redness, an ice-bag. If necessary, hypodermic injections of morphine may be given to relieve the pain. At a later period fomentations may be required to reduce the local inflammation.