Two strains of soil-borne Fusarium solani, both characterized for their ability to produce cyclosporin A and C, were examined for their pathogenicity in severe combined immunodeficiency (SCID) and BALB/c male mice. Intravenous (i.v.) infections with F. solani conidia were performed. No mortality was observed after infection with 0.3-1.6 x 10(7) cfu per mouse in SCID and BALB/c mice. When mice were infected with 0.8-1.5 x 10(6) cfu per mouse and 2 days later with 1.2-1.9 x 10(6) cfu per mouse, 28.6-85.7% survival occurred over a 25-day period, depending on the F. solani strain and the inbred mouse line used. Death was preceded by renal insufficiency affecting both kidneys. Furthermore, i.v. injection with heat-killed conidia followed 2 days later by injecting viable conidia resulted in renal infection in both breeds of mice. F. solani isolated from infected organs was more virulent than the original isolate, and 3/8 (37.5%) of BALB/c and 4/7 (57.1%) of SCID mice died after receiving a single dose. Dissemination to the brain was found only in SCID mice, but torticollis was observed in both mouse breeds. Soil-borne F. solani isolates possess poor pathogenic potential for mice, but either two successive infective doses or a primary injection with heat-killed conidia followed by a single infective dose breaks through host defenses in normal and immunoincompetent mice. Mouse passage increased the pathogenicity of two soil-derived F. solani strains.
