E. coli mastitis – a closer look at the causative bacteria
E. coli is one of the most important causes of mastitis in dairy cattle in the UK. Traditionally, E. coli mastitis has been associated with peracute mastitis but it is now more commonly associated with subacute mastitis without obvious systemic signs and with persistence in the udder after treatment. This suggests that the E. coli strains causing mastitis may have become udder-adapted. However evaluation of phylogeny and the possession of virulence factors suggest that E. coli infection of the udder is simply opportunistic infection by commensal stains of the bacteria which are not specifically adapted to invade or persist in the udder.
Our understanding of coliform mastitis has changed significantly over the past 20 years. From a disease which was perceived as a cause of occasional dramatic acute or peracute mastitis with a very sick cow, E. coli is now recognised as a major cause of persistent subclinical and clinical mastitis in cows without dramatic systemic signs.
E. coli is the commonest facultative anaerobic bacteria in the gut. It is thus constantly excreted into the environment via the faeces. The most amazing thing is not that some get into the udder but that most udders don't get infected. The obvious question is what is it about the bacterial strains that allow them to invade the udder and cause mastitis. Is it just luck – being in the right place at the right time at high enough levels, or are there strains of E. coli which possess specific abilities which allow them to live in the udder?
E. coli isolated from mastitis cases possess a wide range of virulence factors including F17, S and P fimbriae, Afa8 fimbrial adhesin, cytotoxic necrotizing factor 1 and 2, aerobactin and TraT. These virulence factors have been found in many combinations with no one combination predominating. Indeed, most E. coli isolated from mastitis cases possess no virulence factors at all (over 60% in some studies). The genotype of mastitis-causing E. coli is hugely variable and, so far, no link between genotype and mastitis has been found. In addition, this is not just the case for E. coli mastitis in general as the genotype on an individual farm is also hugely variable.
Furthermore, no association between virulence factors and the clinical severity of mastitis has been found. Clearly, the presence or absence of specific virulence factors, such as those which enhance adhesion or epithelial invasion or which damage the host cells, does not determine whether an E. coli strain can cause mastitis, and when it does, it does not determine how severe that mastitis is.
Fig. 1: Peracute E. coli mastitis – no longer the most common form.
E. coli strains can be classified, using PCR, on the basis of their phylogeny – their evolutionary history. A study of 144 E. coli isolated from mastitis cases found that 83% of isolates came from one group. This group consists mainly of strains that have a commensal lifestyle and tend not to be pathogenic in a healthy host. This finding is consistent with the lack of virulence factors in most mastitis isolates, as this group of commensal E. coli tend to lack the specialized virulence traits that characterise pathogenic strains. So again research strongly suggests that there is nothing special about the bacteria which cause E. coli mastitis that differentiates them from the rest of the coliforms coming from the bovine gut.
Apparently recurrent cases of E. coli mastitis after treatment are a relatively common finding – in a study of 300 herds over 10% of cows had recurrent clinical cases. Such cases could be due to reinfection, which is most likely to be with a different strain, or persistence of infection. The 300-herd study showed that both occurred – with the same strain being isolated pre- and post recurrence from half of the cases which recurred in the same quarter. This persistence is, at least, suggestive of udder adaption, which suggests that there may be udder-adapted strains of E. coli. So although most coliform mastitis may be the result of opportunistic infections, a small but important proportion could be caused by adapted pathogens. Early evidence suggested that this may be the case: E. coli strains isolated from persistent cases were often of the same serotype and had the same DNA amplification pattern, while the presence of genes for S and P fimbriae, and specific necrotising factors seemed to be significantly related to persistence of infection after treatment. However, recent data suggests that that association was not true and that no phylogeny or virulence factors are associated with persistence of infection.
E. coli mastitis is an important cause of mastitis on modern dairy farms. The pattern of disease seems to have changed from principally acute toxic mastitis to subacute clinical mastitis. The cause of this change is unclear. The possibility that this is related to changes in the bacteria causing the disease seems unlikely as there is no evidence that virulence factors or bacterial phylogeny are associated with disease severity. Coliform mastitis seems to be the result of opportunistic infection, with no evidence of udder-adapted strains playing an important role even in persistent infections. This highlights once again that prevention of infection from the environment remains key to the control of E. coli mastitis.
Fig. 2: Despite the change in disease presentation, a clean dry environment is still important in preventing coliform mastitis.