Application of experimental results to human problems in poliomyelitis is valid and helpful, especially when the modes of inoculation infection are similar. The disease is spread largely by contact, probably much more often from pharyngeal than from fecal sources. The concept that infection is introduced into and spreads by way of nerve fibers, with multiplication in the nerve cells, appears to explain adequately the various phenomena of the disease, without resort to hypothetic extraneural infection. The usual site of entry is the upper respiratory and alimentary tract, notably the pharynx, rather than the intestine. The usual primary site of infection is probably the peripheral ganglia supplying the upper respiratory and alimentary tracts and the usual primary focus of infection in the central nervous system is probably the lower brainstem, to which many of the earliest and most characteristic clinical manifestations can be traced, particularly to the reticular formation. This nonparalytic form of bulbar poliomyelitis is to be distinguished from the paralytic form. The so-called constitutional symptoms of poliomyelitis are as readily referable to neural infection as to extraneural and presumably are due to the former. In diphasic ("dromedary") cases, the onset of the first phase is essentially of a neurologic, not of a nonspecific or "systemic" character. The diphasic case is regarded as a simple example of remission and relapse. Contributory factors are of two kinds: (1) those that serve to introduce virus into the body; (2) those that increase the severity of already established infection. Avoidance or minimization of these factors is of preventive value.