Congenitally athymic (nu/nu) mice were found to be more susceptible to intravenous challenge with Sporothrix schenckii than their phenotypically normal (nu/+) littermates as measured by lethality and the number of viable yeast cells in the liver 7 days postinfection. Thymus reconstitution of nu/nu mice (nu/thy) conferred a significant degree of resistance to sporotrichosis. Immunization greatly enhanced the resistance of nu/thy and nu/+ mice, but unexpectedly increased the susceptibility of nu/nu mice. The susceptibility of nonimmunized nu/nu mice and the finding that thymus transplants augmented resistance to sporotrichosis suggest that T lymphocytes are critical to host defense.

Syrian hamsters were infected with Sporothrix schenckii by subcutaneous footpad inoculation. Two types of infection could be uniformly induced: a selflimited, lymphatic infection resembling the classical disease in humans, and a generalized nonfatal infection. An infecting dose of approximately 5,300 yeast cells produced the localized subcutaneous-lymphatic disease which was limited to a single limb. In contrast, a 1,000-fold increase in the inoculum temporarily overwhelmed the animals' defense mechanisms, producing a systemic infection involving the liver and spleen. These models were used to demonstrate the development of increased resistance to subsequent infection following either infection or active immunization with ribosomal fractions or trypsinized cell wall antigens of S. schenckii incorporated in Freund complete adjuvant. Agglutination titers were detectable in all animals that were either infected or immunized. In one group of infected animals, the titers persisted for at least 1 year after three booster doses of Formalin-killed S. schenckii. The ability to produce an infection in hamsters which closely resembles the disease seen in humans makes this animal a good model with which to study experimental sporotrichosis.