The objective was to examine effects of treating commercial beef feedlot cattle with therapeutic doses of tulathromycin, a macrolide antimicrobial drug, on changes in the fecal resistome and microbiome using shotgun metagenomic sequencing. Two pens of cattle were used, with all cattle in one pen receiving metaphylaxis treatment (800 mg subcutaneous tulathromycin) at arrival to the feedlot, and all cattle in the other pen remaining unexposed to parenteral antibiotics throughout the study period. Fecal samples were collected from 15 selected cattle in each group just prior to treatment (Day 1), and again 11 days later (Day 11). Shotgun sequencing was performed on isolated metagenomic DNA, and reads were aligned to a resistance and a taxonomic database to identify alignments to antimicrobial resistance (AMR) gene accessions and microbiome content. Overall, we identified AMR genes accessions encompassing 9 classes of AMR drugs and encoding 24 unique AMR mechanisms. Statistical analysis was used to identify differences in the resistome and microbiome between the untreated and treated groups at both timepoints, as well as over time. Based on composition and ordination analyses, the resistome and microbiome were not significantly different between the two groups on Day 1 or on Day 11. However, both the resistome and microbiome changed significantly between these two sampling dates. These results indicate that the transition into the feedlot—and associated changes in diet, geography, conspecific exposure, and environment—may exert a greater influence over the fecal resistome and microbiome of feedlot cattle than common metaphylactic antimicrobial drug treatment.

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Results indicated that environments in veterinary hospitals can be frequently contaminated with S. enterica near where infected animals are managed and fecal specimens containing S. enterica are processed for culture in a diagnostic laboratory. Bacteriologic culture of environmental samples collected with electrostatic wipes is an effective means of detecting contamination in a veterinary hospital environment and may be beneficial as part of surveillance activities for other veterinary and animal-rearing facilities.

Background: There is little information on the duration of nasal shedding of EHV-1 from horses with naturally occurring equine herpesvirus myeloencephalopathy (EHM).Objectives: To evaluate the duration of nasal shedding of EHV-1 in horses affected by EHM. Animals: One hundred and four horses naturally exposed to EHV-1, 20 of which had clinical signs of EHM. Methods: All horses on affected premises were monitored. Those horses developing EHM were sampled in a longitudinal outbreak investigation. Nasal swabs were collected daily from 16 of 20 horses affected by EHM. A qPCR was performed on 98 of 246 nasal swab samples to determine nasal shedding duration. Historical and clinical information was analyzed to evaluate potential risk factors for developing EHM and duration of shedding during this outbreak.Results: The last day shedding was detected in any horse was Disease Day 9. EHV-1 was detected in two-thirds of horses tested on Disease Days 0-3. The amount of EHV-1 DNA found in nasal swabs varied markedly and was not associated with disease severity or age. The odds of developing EHM were greater for febrile horses (OR = 20.3; 95% CI 3.4-390.3; P = .01) as well as for horses attending the riding clinic (OR = 4.1; 95% CI 0.84-21.65; P = .08).Conclusions and Clinical Importance: Biosecurity measures should be implemented for a minimum of 14 days beyond the onset of clinical signs of EHM. Animal managers cannot rely on the severity of clinical signs to predict the duration of EHV-1 shedding.

Measurement of SAA is a more sensitive indicator of inflammation than fibrinogen in the perioperative period of horses requiring exploratory celiotomy for colic. Serial measurement of SAA at 48, 72, and 96 hours after surgery may be helpful to determine risk of complications and guide postoperative management. Measurement of SAA on admission also allows for quantification of SIRS when it is detected clinically.