At the same time recent experience has shown that it requires the greatest care on the part of those having charge of louse destruction to avoid being infected while attending to this duty. The same is true of those examining patients with the disease prior to the eradication of the body lice of the sick.

A knowledge of the life history of the body louse is necessary. The body louse, Pediculus vestimenti, is slightly larger than the head louse, P. capitis, and is the species concerned in the transmission of Indian and North African relapsing fevers as well as typhus fever, although it is probable that the head louse can also transmit these infections.

While the head lice live among the hairs of the head and show their presence chiefly by the appearance of their pear-shaped eggs (nits) projecting from the hair shaft, the body lice attach themselves to the under surface of the garments worn next the skin, and holding fast to the undershirt, feed about twice daily on the human host. They are but rarely found on the skin. The female body louse is about ⅐ inch long and about 1/15 inch broad (3.5 mm. × 1.5 mm.). The antennae are somewhat longer than those of the head louse. Warburton found that the egg stage, in experiments, lasted from eight to forty days, the larval stage about eleven days, and that the male louse lived three weeks and the female four weeks. Of course, under natural conditions these periods may not hold. Development of the eggs takes place best at a temperature of 30°C.

Lice feed at once after being hatched and a young louse will die unless it feeds within 24 hours.

Lice will leave their host only when he has fever or when he dies but they may drop off a host or be brushed off. They are not apt to be found in bedding.

Pathology

Fraenkel, in 1914, first called attention to proliferative changes in the endothelium of the arterioles and arterial capillaries, followed by necrotic changes. These changes are chiefly manifest in the vessels of the skin, central nervous system and myocardium. In addition to the proliferation of the endothelial cells we have a perivascular infiltration of small round cells. Kurt Nicol notes that there is a combination of proliferative and inflammatory changes. These are microscopical and there is absence of characteristic macroscopic findings.

The petechiae are due to thrombosis of the smaller vessels and subsequent haemorrhagic manifestations. Bronchitis and broncho-pneumonia are extremely frequent and form the most common fatal complication. The brain lesions are most common in the basal ganglia, the cerebral cortex and the medulla.

The blood is dark-colored and the liver and kidneys show cloudy swelling. The spleen is somewhat enlarged during the early stages of the disease but tends to be normal in size later on. It is very soft and may rupture while being handled at autopsy. There are no changes in the Peyer’s patches and the mesenteric glands are not enlarged, thus differentiating from typhoid fever. The heart muscle tends to show degenerative changes.