Bayer HealthCare / / Homepage

        deutsch   english
Font size
- 1 2 3 + Font size

click to adjust

Page tools
. Advanced search

Evidence for a specific subset of Escherichia coli bacteria that cause mastitis

Pathogenic Escherichia coli can be classified into several pathotypes, and it is believed that each pathotype carries one or more specific genes that typically involve a number of virulence factors. These genes distinguish them from non-pathogenic E. coli strains and from other pathotypes. Up until recently, it was suggested that this is not the case for E. coli bacteria that cause mastitis. The idea was that any given E. coli isolate can cause this disease, even strains that are considered non-pathogenic. Some recent papers have challenged this concept and make an argument for a specific subset of E. coli bacteria that are more suitable to cause intramammary infections.

Characteristics that may be associated with this specific bovine mammary biotype would include biofilm formation, resistance to Nitric Oxide, resistance to neutrophils, specific bacterial associated molecular patterns (BAMPS) and attachment and invasion of mammary epithelial cells.

In a recent study, eleven Escherichia coli isolates from clinical bovine mastitis cases (mastitic strains) and 11 from the cowshed environment (environmental strains) were compared to determine if the former were a subset of the latter. The mastitic and environmental strains were indistinguishable by O antigen and antibiotic sensitivity. All mastitic isolates showed significantly (P<0.0001) faster growth in milk and faster lactose fermentation than most (approximately 64%) environmental strains. Growth rates in nutrient broth did not differ. The rates of lactose fermentation and growth in milk were positively correlated. Adhesion and phagocytosis of mastitic strains by bovine PMN were significantly (P<0.0001) lower than those of environmental strains, and correlated negatively with growth in milk and lactose fermentation. The average percentages of killing by bovine leukocytes in the two sources were not statistically different. All mastitic strains were serum sensitive, whereas most (approximately 72%) environmental ones were resistant. Finally, pulse-field gel electrophoresis revealed two main pulse type clusters, sharing a similarity coefficient of 79%. Cluster 1 comprised only environmental strains, whereas cluster 2 comprised mostly mastitic strains and only three environmental ones. These results suggest indeed that clinical bovine mastitis E. coli isolates may form a specific subset of the general environmental E. coli population. These mammary pathogenic E. coli (MPEC) seem better able to multiply in the udder medium and to evade the host cellular innate immune response, and are genetically distinct from most environmental strains.

While E. coli mastitis was subjected to extensive epidemiological studies, genetic analysis of MPEC virulence is very limited. This is in sharp contrast with other E. coli pathotypes, which were subjected to extensive genetic analysis. It may be expected that applying extensive genetic evaluations that previously have been used to investigate the virulence of other E. coli pathotypes would be useful in the analysis of MPEC virulence, including identification of putative virulence genes and functional analysis. In the next few years, we expect that a more complete definition of the mammary pathogenic E. coli pathotype will take place.


Blum S, Heller ED, Krifucks O, Sela S, Hammer-Muntz O, Leitner G. Identification of a bovine mastitis Escherichia coli subset. Vet Microbiol. 2008 May 17.

Shpigel NY, Elazar S, Rosenshine I: Mammary pathogenic Escherichia coli. Curr Opin Microbiol. 11:60-65. 2008