Intestinal bacteria are implicated increasingly as a pivotal factor in the development of Crohn's disease, but the specific components of the complex polymicrobial enteric environment driving the inflammatory response are unresolved. This study addresses the role of the ileal mucosa-associated microflora in Crohn's disease. A combination of culture-independent analysis of bacterial diversity (16S rDNA library analysis, quantitative PCR and fluorescence in situ hybridization) and molecular characterization of cultured bacteria was used to examine the ileal mucosa-associated flora of patients with Crohn's disease involving the ileum (13), Crohn's disease restricted to the colon (CCD) (8) and healthy individuals (7). Analysis of 16S rDNA libraries constructed from ileal mucosa yielded nine clades that segregated according to their origin (P<0.0001). 16S rDNA libraries of ileitis mucosa were enriched in sequences for Escherichia coli (P<0.001), but relatively depleted in a subset of Clostridiales (P<0.05). PCR of mucosal DNA was negative for Mycobacterium avium subspecies paratuberculosis, Shigella and Listeria. The number of E. coli in situ correlated with the severity of ileal disease ( 0.621, P<0.001) and invasive E. coli was restricted to inflamed mucosa. E. coli strains isolated from the ileum were predominantly novel in phylogeny, displayed pathogen-like behavior in vitro and harbored chromosomal and episomal elements similar to those described in extraintestinal pathogenic E. coli and pathogenic Enterobacteriaceae. These data establish that dysbiosis of the ileal mucosa-associated flora correlates with an ileal Crohn's disease (ICD) phenotype, and raise the possibility that a selective increase in a novel group of invasive E. coli is involved in the etiopathogenesis to Crohn's disease involving the ileum.

Veterinary Research, a journal on Animal Infection

Staphylococcus aureus is an important cause of udder infections in dairy herds. Both lactational and dry cow therapy are part of Staph. aureus control programs. Reported cure rates for Staph. aureus mastitis vary considerably. The probability of cure depends on cow, pathogen, and treatment factors. Cure rates decrease with increasing age of the cow, increasing somatic cell count, increasing duration of infection, increasing bacterial colony counts in milk before treatment, and increasing number of quarters infected. Staphylococcus aureus mastitis in hind quarters has a low cure rate compared with front quarters. Antimicrobial treatment of intramammary infections with penicillin-resistant Staph. aureus strains results in a lower cure rate for treatment with either beta-lactam or non-beta-lactam antibiotics. Other strain-specific factors may affect the probability of cure but routine diagnostic methods for use in bacteriology laboratories or veterinary practices are not yet available. The most important treatment factor affecting cure is treatment duration. Increased duration of treatment is associated with increased chance of cure. Economically, extended treatment is not always justified, even when indirect effects of treatment such as prevention of contagious transmission are taken into consideration. Usefulness of treatment trials could be improved by standardization of case definitions, consideration of host and strain factors, and sufficient statistical power. Treatment of young animals with penicillin-sensitive Staph. aureus infections is often justified based on bacteriological cure and economic outcome, whereas treatment of older animals, chronic infections, or penicillin-resistant isolates should be discouraged.

This paper investigates the impact of lameness on milk yield. The dataset includes approximately 8000 test-day milk yields from 900 cows on five farms in Gloucester, UK, collected over 18 mo from 1997 to 1999. The data were structured to account for repeated measures of test-day yield (1 to 10 per cow) and analyzed to account for this autocorrelation. Factors affecting milk yield included: farm of origin, stage of lactation, parity, and whether a cow ever became lame. In clinically lame cows, milk yield was reduced from up to 4 mo before a case of lameness was diagnosed and treated and for the 5 mo after treatment. The total mean estimated reduction in milk yield per 305-d lactation was approximately 360 kg. We conclude that clinical lameness has a significant impact on milk production. This is important information for assessing the economic impact of clinical lameness and its impact on cow health. It adds weight to the importance of early identification of clinical lameness and the urgency of techniques to improve the definition of this highly subjective diagnosis.

Mastitis, inflammation of the mammary gland, can be caused by a wide range of organisms, including gram-negative and gram-positive bacteria, mycoplasmas and algae. Many microbial species that are common causes of bovine mastitis, such as Escherichia coli, Klebsiella pneumoniae, Streptococcus agalactiae and Staphylococcus aureus also occur as commensals or pathogens of humans whereas other causative species, such as Streptococcus uberis, Streptococcus dysgalactiae subsp. dysgalactiae or Staphylococcus chromogenes, are almost exclusively found in animals. A wide range of molecular typing methods have been used in the past two decades to investigate the epidemiology of bovine mastitis at the subspecies level. These include comparative typing methods that are based on electrophoretic banding patterns, library typing methods that are based on the sequence of selected genes, virulence gene arrays and whole genome sequencing projects. The strain distribution of mastitis pathogens has been investigated within individual animals and across animals, herds, countries and host species, with consideration of the mammary gland, other animal or human body sites, and environmental sources. Molecular epidemiological studies have contributed considerably to our understanding of sources, transmission routes, and prognosis for many bovine mastitis pathogens and to our understanding of mechanisms of host-adaptation and disease causation. In this review, we summarize knowledge gleaned from two decades of molecular epidemiological studies of mastitis pathogens in dairy cattle and discuss aspects of comparative relevance to human medicine.

Incidence of clinical mastitis was studied in 274 herds grouped in three categories by bulk milk somatic cell count (SCC). Mean incidence rate of clinical mastitis was 0.278, 0.257, and 0.252 cases per 365 cow-days at risk in herds with low (< or = 150,000), medium (150,000 to 250,000), and high (250,000 to 400,000 cells/ml) bulk milk SCC, respectively. The incidence rate of clinical mastitis was not different among the three categories. Variance in the incidence of clinical mastitis among herds increased as bulk milk SCC decreased. Clinical mastitis caused by Gram-negative pathogens, such as Escherichia coli, Klebsiella spp., or Pseudomonas spp., occurred more often in herds with a low bulk milk SCC. Clinical mastitis caused by Staphylococcus aureus, Streptococcus dysgalactiae, and Streptococcus agalactiae occurred more often in herds with a high bulk milk SCC. Systemic signs of illness caused by clinical mastitis occurred more often in herds with a low bulk milk SCC. Both overall culling rate and culling rate for clinical mastitis were not different among groups catergorized by bulk milk SCC. In herds with a high bulk milk SCC, however, more cows that produced milk with a high SCC were culled. In herds with a low bulk milk SCC, more cows were culled for teat lesions, milkability, udder shape, fertility, and character than were cows in herds with a high bulk milk SCC. In herds with a low bulk milk SCC, cows were also culled more for export and production reasons.