The development of Hymenolepis diminuta (Cestoda: Cyclophyllidea) as affected by a preexisting H. diminuta infection was studied, and the fate of worms in crowded infections was determined after periods up to 5 months. When rats with mature primary infections of various intensities are superinfected with 10 cysticercoids, and the worms recovered 10 days after secondary infection, weights of individual secondary worms are inversely proportional to the numbers of primary worms present. Secondary worm recovery is slightly lower with increasing numbers of primary worms, but many secondary worms establish themselves in all cases studied. When rats with secondary infections are followed for longer periods, secondary worms eventually increase in size and merge indistinguishably with the primary population, whether the primary infection is of low density or crowded. However, initial growth rate of secondary worms is depressed and maturation is delayed. When crowded (50 cysticercoids/rat) infections are followed up to 5 months, there is often a spontaneous loss of part of the infection. Available evidence for the existence of premunition in cestode infections is reviewed, and avoidance of the term "premunition" with reference to lumen-dwelling cestodes is suggested. "Premunition" is defined as ". .. a state of resistance to infection which is established after an acute infection has become chronic and which lasts as long as the infective organisms remain in the body" (Dorland's Illustrated Medical Dictionary, 1965), and by Sprent (1963) as ". .. a relative resistance which is dependent upon the host remaining a carrier of infection and which is not accompanied by abundant antibodies." Sprent (1963, p. 80) preferred the term "co-infectious immunity" to describe the phenomenon. Authors of texts, reference works, and reviews have often accepted the existence of premunition in cestode infections in the sense of protection against superinfection (Culbertson, 1941; Hyman, 1951; Larsh, 1945; Smyth, 1962; Swellengrebel and Sterman, 1961; Wardle and McLeod, 1952; Watson, 1960; Weinmann, 1966). These authors agree that the phenomenon does not involve host antibody response, but that the protection is due in some way to crowding. The existence of a crowding effect, i.e., that increased numbers of cestodes in the host results in smaller individual worm size in H. diminuta, is well established (Read, 1959; Roberts, 1961, 1966). The size of the worms is approximately in inverse proportion to the number present. The relationship is described Received for publication 21 June 1967. * This investigation was supported by Grant AI06153 from the NIH, U. S. Public Health Service. by a rectangular hyperbola (Read, 1959; Read and Simmons, 1963). Available experimental evidence supporting the assertion that premunition occurs in cestode infections consists of the following: In a single attempt, Palais (1934) reported failure to superinfect a rat with Hymenolepis diminuta. Chandler (1939), in a series of experiments with H. diminuta, concluded that (1) the percentage establishment of the secondary worms is in inverse proportion to the number of primary worms already in the host, and the presence of 36 primaries precluded secondary worm establishment; (2) establishment of secondaries is not decreased by the presence of 7or 10-day-old primaries, but is inhibited by 14-day-old primaries; (3) size of secondaries is decreased by the presence of primaries as compared to previously uninfected controls (at 10 days after secondary infection) and is in inverse proportion to numbers of primaries present; and (4) since establishment and growth of secondary worms was normal in rats from which the primaries had been chemically or mechanically removed, the aforementioned inhibitory effects were due to crowding rather than host antibody response. In view of the apparently wide acceptance of the premunition phenomenon in cestodes and the lack of extensive experimental evidence for it, we undertook the experiments described below. Since Chandler did not follow worm growth further than 10 days after secondary infection, we determined the ulti-