The incidence of Pythium spp. and Aphanomyces cochlioides associated with the sugar-beet growing soils of Britain

In a survey of fungi causing seedling diseases of sugar beet using a soil bioassay, Aphanomyces cochlioides and Pythium spp. were found to occur in 39% and 31%, respectively, of 341 sugar-beet fields selected in a stratified random sample in England. The frequency of A. cochlioides-infested soils varied widely in the different sugar-beet growing areas of the country. Soil pH was the single factor most strongly associated with the distribution of the pathogen, but regression models applied to combinations of factors indicated that soil texture and the interval between sugar-beet crops were also relevant to its frequency. It was detected less often in soils of high pH (greater than or equal to 7.5), heavy texture and where the interval between sugar-beet crops exceeded 5 years. No significant associations were found between the proportion of soils with Pythium spp. and soil or cropping factors

Do type 1 fimbriae promote inflammation in the human urinary tract?

Type 1 fimbriae have been implicated as virulence factors in animal models of urinary tract infection (UTI), but the function in human disease remains unclear. This study used a human challenge model to examine if type 1 fimbriae trigger inflammation in the urinary tract. The asymptomatic bacteriuria strain Escherichia coli 83972, which fails to express type 1 fimbriae, due to a 4.25 kb fimB-fimD deletion, was reconstituted with a functional fim gene cluster and fimbrial expression was monitored through a gfp reporter. Each patient was inoculated with the fim+ or fim- variants on separate occasions, and the host response to type 1 fimbriae was quantified by intraindividual comparisons of the responses to the fim+ or fim- isogens, using cytokines and neutrophils as end-points. Type 1 fimbriae did not promote inflammation and adherence was poor, as examined on exfoliated cells in urine. This was unexpected, as type 1 fimbriae enhanced the inflammatory response to the same strain in the murine urinary tract and as P fimbrial expression by E. coli 83972 enhances adherence and inflammation in challenged patients. We conclude that type 1 fimbriae do not contribute to the mucosal inflammatory response in the human urinary tract