Bovine digital dermatitis (BDD) is an infectious claw disease chiefly induced by treponemes, while deep digital sepsis (DDS) is caused by pyogenic bacteria. It is currently unclear why persistent BDD-associated claw horn lesions (BDD-CHL) do not develop DDS. One possible explanation could be that the intralesional presence of treponemes makes it more difficult for pyogenic bacteria to colonize BDD-CHL. To lay the groundwork for exploring this possibility, we determined the presence and amounts of treponemes and selected pyogenic bacteria in BDD-CHL versus DDS at the DNA level. “Total Treponema” (TT-)PCR and type-specific qPCR were used to screen 18 BDD-CHLs from 15 cows and 18 DDS samples from 11 cows for bacterial DNA. TT-PCR identified Treponema DNA as most abundant DNA in 8/18 BDD-CHLs and 1/18 DDS samples. qPCR revealed Treponema pedis DNA in all BDD-CHLs, and one DDS lesion. Fusobacterium necrophorum DNA was significantly more abundant in DDS compared to BDD-CHL samples (p = 0.027). Both lesion types harbored similar mean levels of Trueperella pyogenes DNA. Interestingly, 7/18 DDS samples contained Parvimonas DNA. Our DNA-based data call for downstream studies involving living BDD-CHL-associated Treponema species and F. necrophorum, and, importantly, point to a possible pathogenic role of Parvimonas in DDS.
Brandt et al. (Wed,) studied this question.
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