FOUR FIGURESEven a casual inspection of the palmar and plantar surfaces suffices to demonstrate that there are regional variations in the breadths of epidermal ridges. Ridges of the sole are generally coarser than those of the hand (Galton, 1892) ; variations in different regions are apparent in the hand and foot alike, the prominent distinction being increased ridge breadth in the proximal territories. When corresponding regions of different individuals are compared it is observed that ridges tend to be coarser in men than in women, that they coarsen in prenatal and postnatal growth, and that some differences occur among individuals of the same sex and body size. Curiously enough, the literature contains little more than casual statements on the subject of ridge breadth, most often presented as in this brief introductory comment without quantitative data.The most extensive available information relates to the growth of ridges : Kolliker (1848-1849), Kollmann (1883), A. F. Hecht ( '24). The findings of these authors are in close agreement, and Hecht 's figures are cited as representative. The following are average breadths of single ridges, in fingertip patterns alone: three premature infants 0.15 mm.; seven newborn infants 0.18 mm. ; then, without giving the numbers of subjects involved, 10 years 0.30-0.35 mm.; adult women 0.40-0.50 mm. ; adult men 0.50 mm. It will be noted that Hecht 127

Mice depleted of T-lymphocytes by thymectomy and irradiation (TXB) and immunologically competent mice were compared for gross and histological pathology as well as immune responses after cutaneous and/or intravenous challenge with Candida albicans. In response to a first cutaneous inoculation with viable Candida, TXB, sham-operated (SXB), and unmanipulated (normal) mice, all developed lesions of comparable size, duration, and histopathology. When challenged a second time cutaneously, normal and SXB mice developed lesions which were greatly increased in size when compared with those produced by a first cutaneous infection, whereas TXB mice developed lesions comparable in size to those initiated by the first infection. Histologically, the first and second lesions in all animals were acute abscesses predominantly comprised of polymorphonuclear leukocytes. The larger second lesions in SXB and normal mice were accompanied by detectable circulating antibody and by delayed hypersensitivity. Neither circulating antibody nor delayed hypersensitivity were stimulated in the TXB mice. When challenged intravenously, all previously uninfected mice, regardless of T-cell status, were equally susceptible to C. albicans. Contrary to SXB or normal mice, however, TXB mice which had been infected cutaneously were not more resistant to a subsequent intravenous challenge as judged by 6-week survival. The results suggest that T-cells do not play a significant role in innate resistance of mice to systemic candidiasis, but that such cells are important in the development of acquired resistance.Candida albicans (Robin) Berkhout is a fungus which does not usually invade the normal host, although it is a member of the normal human microbial flora. The mechanism by which healthy individuals resist invasion is unclear, but it is generally believed that cell-mediated immunity, and thus the T-lymphocyte, is an important factor in acquired resistance. The latter statement is based primarily on clinical evidence, in that individuals with immunodeficiency diseases (3,18,22,32,35) or with diseases for which the treatment itself is immunosuppressive (1, 17, 20, 24, 28, 37) are particularly susceptible. Experimental evidence to corroborate the clinical evidence is somewhat meager.Recently, however, a natural model of immunological modification, viz., the nude or athymic mouse, has been used to investigate innate resistance to C. albicans. Cutler (10) inoculated nude mice with large doses of C. albicans intravenously and observed that such mice were more t Present address: Mt. Sinai Hospital, Department of Microbiology, New York, NY 10029.

Cutaneous infection of mice with Candida albicans elicited a predominantly acute inflammatory response, stimulated the production of precipitating antibodies, and conferred protection against subsequent intravenous challenge with the same organism. The acute inflammatory skin reaction seen after cutaneous infection suggested a predominantly humoral response to Candida. Animals infected cutaneously a second time with viable C. albicans developed larger skin lesions than animals infected only once, and the twice-infected animals were more resistant to an intravenous challenge as well. The cutaneous inoculation of mice with heat-killed C. albicans was less effective in stimulating antibody production, in eliciting the inflammatory response, and in inducing a protective response demonstrable by intravenous challenge with viable Candida. This model of experimental candidiasis represents a reproducible means of studying a protective immune response to the organism. times with nonpyrogenic physiological sodium chloride (NPS) (Cutter Laboratories, Berkeley, Calif.). More than 95% of the cells in such suspensions were blastospores. The cells were then quantitated in a hemacytometer, and the counts were verified by diluting and plating the same suspensions with which animals were inoculated. Killed cells for animal inocula-499 on July 16, 2020 by guest http://iai.asm.org/ Downloaded from on July 16, 2020 by guest http://iai.asm.org/ Downloaded from

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