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Summary 1.Faecal pellet group (FPG) count data are widely used to estimate animal abundance, with two alternative methods normally employed. Faecal accumulation rate (FAR) techniques measure the daily accumulation rate of pellet groups, while faecal standing crop (FSC) techniques measure overall density. To estimate abundance, both methods require estimates of the animal defaecation rate. FSC techniques also require an estimate of pellet group decomposition rate. In general, FAR techniques are considered less prone to bias while FSC methods are considered more precise and cost-effective. On balance, the majority of authors and practitioners prefer FSC methods, although little empirical evidence supports this decision. 2. FPG count data were obtained from 26 study areas to compare the precision of FAR and FSC count techniques when applied to wild deer populations in the UK uplands. The time needed to collect count data was quantified in 10 study areas. 3. The coefficients of variation (CV) of FSC pellet group count data ranged from 9% to 23% and were approximately 0·7-0·9 times those of equivalent FAR data. The precision of both methods was related to the density of pellet groups. On average, FSC count data took 80 min per plot to obtain, with FAR taking 1·6-1·9 times longer. 4. For the precision of FSC and FAR abundance estimates to be comparable in the range of conditions studied, decomposition rate trials would require a CV of 5-20%. While a number of studies report this to be possible, estimates of the time needed to obtain this level of precision generally exceed the net available time that results from the deployment of FSC rather than FSC pellet group counts. 5. Synthesis and applications . Using the levels of finance available to most deer managers in the UK uplands, deer abundance estimates obtained using FSC techniques on individual study sites up to 20 000 ha appear generally less cost-effective than FAR when compared in terms of their overall precision. As FAR methods are also thought to have less potential for bias when applied in the appropriate environmental conditions, they should be preferred over FSC when estimating deer abundance in concealing habitats.

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Recent transposon mutagenesis studies with two enterohemorrhagic Escherichia coli (EHEC) strains, a serotype O26:H-strain and a serotype O157:H7 strain, led to identification of a putative fimbrial operon that promotes colonization of young calves (1 to 2 weeks old). The distribution of the gene encoding the major fimbrial subunit present in O-island 61 of EHEC O157:H7 in a characterized set of 78 diarrheagenic E. coli strains was determined, and this gene was found in 87.2% of the strains and is therefore not an EHEC-specific region. The cluster was amplified by long-range PCR and cloned into the inducible expression vector pBAD18. Induced expression in E. coli K-12 led to production of fimbriae, as demonstrated by transmission electron microscopy and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. The fimbriae were purified, and sera to the purified major subunit were raised and used to demonstrate expression from wild-type E. coli O157:H7 strains. Induced expression of the fimbriae, designated F9 fimbriae, was used to characterize binding to bovine epithelial cells, bovine gastrointestinal tissue explants, and extracellular matrix components. The fimbriae promoted increases in the levels of E. coli K-12 binding only to bovine epithelial cells. In contrast, induced expression of F9 fimbriae in E. coli O157:H7 significantly reduced adherence of the bacteria to bovine gastrointestinal explant tissue. This may have been due to physical hindrance of type III secretion-dependent attachment. The main F9 subunit gene was deleted in E. coli O157:H7, and the resulting mutant was compared with the wild-type strain for colonization in weaned cattle. While the shedding levels of the mutant were reduced, the animals were still colonized at the terminal rectum, indicating that the adhesin is not responsible for the rectal tropism observed but may contribute to colonization at other sites, as demonstrated previously with very young animals.Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 causes gastrointestinal disease in humans that can be life threatening as a consequence of Shiga toxin activity on kidney and brain vasculature. Ruminants, particularly cattle, are the primary reservoir hosts for this organism (1, 3). Cattle are colonized without any overt symptoms and can shed EHEC O157:H7 in their feces for several weeks at levels up to 10 6 cells per g. Recent work has demonstrated that the predominant colonization site in cattle for E. coli O157:H7 is the final few centimeters of the terminal rectum, a site having a high density of lymphoid follicles and lymphoid-associated mucosa (19,21,30). A key aim of our research is to identify bacterial factors that drive this tropism for the terminal rectum.Considerable attention has been focused on type III secretion that leads to intimate attachment, and this has been shown to be important for ruminant colonization in a number of studies (5,7,8,22,44). For example, in a recent signaturetagged mutagenesis (STM) screening for genes that promote E. col...

Following peripheral exposure, many transmissible spongiform encephalopathy (TSE) agents accumulate first in lymphoid tissues before spreading to the CNS (termed neuroinvasion) where they cause neurodegeneration. Early TSE agent accumulation upon follicular dendritic cells (FDCs) in lymphoid follicles appears critical for efficient neuroinvasion. Most clinical cases of variant Creutzfeldt-Jakob disease have occurred in young adults, although the reasons behind this apparent age-related susceptibility are uncertain. Host age has a significant influence on immune function. As FDC status and immune complex trapping is reduced in aged mice (600 days old), we hypothesized that this aging-related decline in FDC function might impair TSE pathogenesis. We show that coincident with the effects of host age on FDC status, the early TSE agent accumulation in the spleens of aged mice was significantly impaired. Furthermore, following peripheral exposure, none of the aged mice developed clinical TSE disease during their lifespans, although most mice displayed histopathological signs of TSE disease in their brains. Our data imply that the reduced status of FDCs in aged mice significantly impairs the early TSE agent accumulation in lymphoid tissues and subsequent neuroinvasion. Furthermore, the inefficient neuroinvasion in aged individuals may lead to significant levels of subclinical TSE disease in the population.