ranging from 1 to 7 weeks of age. Five-week-old (31-36 days) neonates demonstrated waning resistance by the appearance of typically ulcerative, progressive lesions, though their parameters (duration, size) were not yet those of adult control lesions. The resistance demonstrated by neonates may be due in part to group housing (nesting) which could create unfavorable temperatures for T. pallidum survival; comparison of lesion development between nesting and individually housed neonates, 31 to 46 days of age, revealed a greater percentage of typical lesions developing among those individually housed (95 versus 52%). However, these differences may reflect the variability of typical lesion develop ment found among animals of this age when resistance begins to wane. In both groups, the duration of typical lesions was significantly shorter than for adult controls. A heat-stable serum factor(~) was demonstrated in 19 of 20 basal sera from neonates 4 to 6 days of age; this presented another possible mechanism of resistance. The neutralizing serum factor(s) was not demonstrable in the sera of does either before mating, during gestation, or shortly after kindling. The relationship of temperature, serum 1 966 GAMBOA AND MILLER factors, and nutritional factors to neonatal resistance following infection, which begins to subside as the animal reaches 5 weeks intradermal inoculation with T. pallidurn is discussed.of age. The potential influences of nesting and serum neutralizing factors upon resistance are advanced. Abbreviations W R L , Venereal Disease Research Laboratory NRS, nonimmune rabbit serum IRS, immune rabbit serum Micro-NZ, microneutralizationThe advent of penicillin therapy brought about a dramatic reduction in the incidence of congenital syphilis (12,34,39). However, the decline in both the use of routine screening procedures and physicians' training programs has resulted in the reemergence ofthis form of the disease as a public health problem (2, l I, 34, 38, 46, 49, 50, 60). Despite this problem, little is known about the interacting events associated with the organism and host which determine infectivity. Since the recognition of congenital syphilis as a distinct clinical entity, it has been generally accepted that treponemes cross the placenta only after the 4th month of gestation, at a time when the Langhans cell layer (cytotrophoblast) becomes atrophied (20). Recent evidence, however, indicates that treponemes can be found in conceptus material obtained during the first trimester (21). Silverstein and Lukes (43) and Silverstein (42) have suggested that infection during early gestation may go undetected due to the absence of an inflammatory reaction attributed to the immaturity of the fetal immune system. The introduction of Treponerna pallidurn from an infected mother to fetus may result in either a fulminating fatal disease, latency, or the absence of infection; factors which influence the outcome are not understood. The lack of a satisfactory and reproducible experimental rabbit model has precluded stud...