Winter dysentery

By CS McConnel, Veterinary Medicine Extension

In February of last year, the FDIU group worked with a dairy that was experiencing an outbreak of winter dysentery in their lactating cattle. On that farm the progression of disease moved from one freestall barn to the next over the course of approximately one week. There did not seem to be any mortality associated with the outbreak, but widespread morbidity primarily manifested as diarrhea with a notable drop in average milk production. There was substantial feed wastage due to inappetence and concerns that lasting effects might be observed in both reproductive efficiency and milk production persistence. In conversations with management, it was noted that older cows seemed more resistant to the disease which was attributed to possible residual immunity due to a prior outbreak approximately five-years earlier.

In fact, this particular farm has a history of adult cow winter dysentery occurring over a roughly five-year cycle. Bovine coronavirus (BCoV) is the causative agent of winter dysentery in adult cattle, and the reoccurring nature of these outbreaks raised the question as to whether there are any viable preventive options. It also brought up a question regarding BCoV variants given that the preweaned calves have evidence of circulating BCoV on a regular basis. That relatively consistent exposure would seemingly provide ongoing immunologic protection that would be expected to limit adult cow outbreaks to novel, dominant variants affecting diverse age groups rather than younger lactating animals only.

Given these questions, we decided to dig into the literature for answers. Interestingly, there appears to be relatively little recent research into BCoV variants underlying winter dysentery within the US. There are some reports from overseas, including a 2021 Israeli study (Viruses 2021, 13(6)) that demonstrated selective pressure that might affect viral-host interactions. However, the authors of that study stated that the effect of amino acid variations found in local strains on viral virulence and host response, and in particular, their effect on the protective immunity of adult cattle, needs to be tested by future studies.

Perhaps the most informative recent article regarding BCoV and associated diseases was published in 2021 in Frontiers in Veterinary Science (Sec. Veterinary Infectious Diseases, Vol. 8). The authors of that article pointed out that no distinct genetic or antigenic markers have been identified in BCoVs associated with the three distinct clinical syndromes in cattle: (neonatal) calf diarrhea, winter dysentery, and respiratory infections. In fact, all BCoV isolates identified so far are shed in feces and nasal secretions and belong to a single serotype/genotype based on virus cross-neutralization and genotyping analyses regardless of clinical origin. However, genotyping has identified distinct sublineages and clusters based on the year and place of isolation but not on the disease type. In other words, no genetic or antigenic markers associated with the different disease manifestations have been identified, suggesting that the latter may result from the complex interplay between pathogens (BCoV and other viruses or bacteria), host and environmental factors. Overall, the authors of the Frontiers’ article stated that the complex interactions between BCoVs, their cellular receptors and mucosal microbiota need to be comprehensively evaluated to improve our understanding of BCoV epidemiology, pathogenesis and interspecies transmission.

But what about preventing winter dysentery? And what about herd immunity? Well, according to the Frontiers’ article there is evidence to suggest that an active immune response to BCoV does not always result in viral clearance. Although most cases of BCoV-induced enteritis occur within the first 30 days of life, low-level intermittent BCoV shedding can be observed in >70% of healthy cows despite the presence of serum and intestinal BCoV-specific antibodies. Furthermore, because BCoV is more stable at lower ambient temperature and reduced ultraviolet light levels, BCoV shedding rates increase by 50–60% during the winter months which likely contributes to the development of winter dysentery in adult cattle. BCoV shedding has also been shown to increase by 65% at parturition, and by 71% two weeks postpartum due to immunological and hormonal perturbations in cows. Ultimately, the correlates of immune protection against BCoV infections remain poorly defined. Most vaccines against mucosal pathogens fail to induce sterilizing immunity or to prevent subsequent reinfections, as observed for natural or experimental BCoV infections. Further studies are needed to determine whether inclusion of a mixture of calf diarrhea/winter dysentery/respiratory infection strains could be an optimal strategy to develop a single broad-spectrum BCoV vaccine effective against BCoV infections associated with distinct clinical syndromes. As it stands, observational data and field studies are scarce for the evaluation of protective efficacy against winter dysentery from currently licensed modified live vaccines against BCoV. The bottom line is that the complexity of vaccine management (the need to target variable age groups of cattle, production status, newly arriving animals, etc.) and a suboptimal cost-benefit ratio of vaccine use suggest that alternative biosecurity-based control and prevention strategies need to be evaluated and employed. Unfortunately, the limited options for prevention means that if you are faced with an outbreak of winter dysentery in the coming months your only option may be to try and slow rather than stop the spread.