Dr. Johnson has a long-standing interest in investigating microbial uropathogenicity factors using animal models of urinary tract infection (UTI). He has focused intensively upon Escherichia coli (causes the great majority of uncomplicated community-acquired UTIs and remains a prominent cause of hospital-acquired bacteremia from a UTI); Proteus  mirabilis (sometimes the most common isolate from urine of patients with compromised urinary tracts, including urinary diversions, urethral catheters, condom catheters, suprapubic catheters or intermittent catheterization) and Candida glabrata (nosocomial Candida UTIs have increased two- to four-fold in recent years and now constitute the cause of 20-30% of nosocomial UTIs. 

He has adapted and significantly modified a mouse model of urinary tract infection described by Hagberg, et al.(Infect. Immun. 1983. 40:273). The mouse model permits examination of the interplay of microbial in vivo expression of virulence factors with the host target organ and defensive response.  The model has been developed and used specifically to study the pathogenesis of acute pyelonephritis and cystitis and has several appealing features including minimal manipulation, no obstruction to urine flow, receptors for type 1 and P fimbnae of E. coli, distinctions among pyelonephritogenic, cystogenic, and fecal E. coli strains, a natural predisposition to P. mirabilis UTI, and susceptibility to C. glabrata infection.

He has used this mouse model to: develop a short-term and a long-term bladder catheter model, describe the effect of urethral obstruction on the uropathogenicity of a "nonuropathogenic" E. coli strain, observe the role of E. coli P fimbriae in acute pyelonephritis, assess the contribution of MR/P fimbriae and of flagella to the uropathogenicity of P. mirabilis, document the contribution of urease expression to the uropathogenicity of P. mirabilis, determine that PMF fimbriae contributes to bladder more than kidney colonization of P. mirabilis, define in vivo differences between uropathogenicity of cystitis and pyelonephritis E. coli strains, describe a model of C. glabrata UTI, use green fluorescent protein to track P. mirabilis urease gene expression in vivo, observe in vivo phase variation of MR/P and Type 1 fimbriae, determine immune response to and protection offered by P. mirabilis vaccine candidates, and discover virulence genes interrupted by signature tagged mutagenesis.