In a Canadian study published in the July 2017 issue of Journal of Dairy Science, researchers compared a quaternary ammonium compound-based (QAC) footbath to a more conventional copper sulfate (CuSO4) footbath. Five farms used a standard 5% footbath concentration of CuSO4. Another five farms used a 1% footbath concentration of QAC (per the manufacturer’s recommendation). An additional five farms that did not alter their standard hoofcare routine were also included. These dairies averaged 143 cows and a prevalence of active digital dermatitis (DD) lesions (hairy warts) of 15%. The protocols for the CuSO4 and QAC interventions had cows walking through freshly prepared footbaths once a day after milking Monday–Friday for 12 consecutive weeks.
In the CuSO4 group, the prevalence of chronic DD lesions decreased over the 12 weeks of the study. For the QAC group, chronic DD lesion prevalence decreased at the same rate for weeks 0–6, but then leveled off between 6 and 12 weeks. The QAC treatment also did not decrease the proportion of cows with active DD lesions. The researchers concluded that QAC was inferior to CuSO4 for footbath control of hairy warts. This is unfortunate, as a viable alternative to CuSO4 would be useful to reduce the amount of copper that ends up in pastures and crop fields (via manure handling and application systems).
Sunrise, sunset. When to eat, when to sleep. Like people and plants (and microbes!), cows have a circadian pattern. Circadian rhythms are the physiological and behavioral changes that follow a predictable pattern over the course of a day.
In a recent study, the exact locations of 350 cows in a free-stall barn on a Danish dairy were tracked each second for 5 months using a real-time positioning system (GEA’s CowView). Cows were classified as resting (in a stall), feeding (at the feed bunk), or in alley (in the milking robot or otherwise not in a stall or eating). Each of these activities was weighted: resting was negative (-0.15), feeding was very positive (+0.34), and in alley was less positive (+0.12). Then these weights were applied to the number of hours each cow spent doing each activity, which resulted in an average activity level across the herd over the day (see solid lines in the figure for “normal” cows).
That cows have circadian rhythms, shaped by light-dark cycles and management activities (like stall cleaning), is no surprise. What is interesting, is that the researchers found that circadian patterns changed when a cow was feeling poorly (lameness or mastitis) or coming into heat (see dashed lines in the figure). Lame cows showed less overall activity level variation over the course of the day. Cows with mastitis showed higher activity during the day but lower activity into the evening.
What’s more interesting is that the shift in circadian pattern occurred 1 to 2 days before the farmer detected the abnormality. These results should be verified in other settings with additional diagnostic tools. However, monitoring circadian patterns of activity may serve as an early warning system for cows that may require additional attention.
We hate it when it happens, but sometimes cows (and heifers and calves) die on the farm. Along with the economic loss is the hit to morale. Mortality losses average 6-8% in U.S. dairy herds, which is higher than 40 years ago. Systematic collection and analysis of death information may help prevent other deaths in the future and improve overall welfare of the herd.
The Integrated Livestock Management program at Colorado State University’s vet school has a Certificate of Death form for dairy cattle. The purpose is to record detailed information about each animal’s death in order to improve overall health management. The form includes spots for the expected items like id, birth date, calving date, and death date, but also things like body condition score, days in milk, and calving ease score. The section for cause of death doesn’t have just one line, it has space to write in the conditions that led to the cow’s final demise. Did she have a metabolic imbalance? An infection? An injury from a piece of equipment? Identifying the timeline of contributing events allows for an assessment of health risks on the dairy. Causes that appear frequently in death certificates should serve as a call to action. The authors of the form advise using a coding system that allows for a more detailed cause of death to be included in the cow’s individual record.
The folks at Colorado State University have also written a Dairy Cattle Necropsy Manual that includes illustrated, step-by-step directions for conducting an on-farm necropsy. The manual has lots of photos of both normal organs and commonly found abnormalities. There is also guidance for taking tissue samples. When doing a “home” necropsy, take plenty of pictures for the subsequent conversation with your veterinarian.
Completing certificates of death for cows, heifers, and calves provides the necessary information for analyzing health management practices so that improvements can be made and mortality rate decreased. Information may be the only thing of value that comes from an animal’s untimely death. Let’s use it.
We know that hornless cattle are safer for people, their herdmates, and themselves. Unfortunately, the combination of polledness and elite genes for other, more critical traits (like milk yield and productive life) don’t often appear in the same animals. We could spend several decades using polled sires to introgress the POLLED allele (allele = version of a gene) into the broader dairy population, but we would sacrifice gains in other traits, because along with the POLLED allele, the calves would get other stretches of less desirable DNA. (However, the nice thing about the POLLED allele is that it’s dominant, meaning that only one POLLED allele is required. At that same location on the other paired chromosome, there can be the horned allele, but we would still have a polled cow.)
You may have heard of gene editing, particularly with a system called CRISPRs. These CRISPR molecules can be introduced into target cells and are capable of recognizing a particular stretch of DNA and cutting at that location. If pieces of DNA containing the desired sequence for that location (e.g., the POLLED sequence) are made available to the cell at the same time, the cell’s DNA repair machinery will use that “new” DNA to repair the break in the chromosome. Voila! That repaired chromosome now contains the DNA sequence we want at that location, instead of the sequence that was originally there.
This type of gene editing has been successfully done in cattle embryos. In this case, the researchers used a more primitive version of CRISPRs called TALENs, but they do the same thing. In embryonic cells from horned cattle, the targeted section of DNA on chromosome 1 was replaced with the POLLED DNA sequence. In this proof-of-concept experiment, clones were created from these cells. And they grew no horns! The rest of the DNA in these animals remained the same as it was in the original genetic source, only the horned/polled location was altered. The two bulls produced (pictured above) will be used in breeding experiments to confirm that their offspring will also be polled.
This precise gene editing technique could be used to introduce polledness into elite dairy sires. In one generation, we could nearly eliminate the need to dehorn/disbud calves. That’s assuming there are no regulatory setbacks regarding the gene editing technology. (Ah, the potential sticking point.)
If you’d like some additional explanation accompanied by video of the polled bulls—currently residing at UC Davis—Science Friday has that here. The paper can be found here on page 479 (Carlson et al. 2016 Nature Biotechnology 34:479-481). I’ve glossed over some of the details, so if you’d like any additional explanation, please post a question via the “Leave a reply” link or email me.
Cattle, like people, can get vitamin D from food and from exposure to the sun. Specifically, vitamin D2 is acquired from plants, while vitamin D3 is synthesized by cells in sun-exposed skin. Vitamin D availability within the body is often measured as the concentration of 25(OH)D in the blood (serum). 25(OH)D is a product of metabolism of both vitamins D2 and D3. With summer sun exposure and no exogenous vitamin D, cows will have 40-100 ng/mL serum 25(OH)D. For cows without the opportunity to graze out on the range all summer, alfalfa hay can provide pretty significant amounts of vitamin D2, and even corn silage contains some. Additionally, vitamin-mineral supplement mixes usually contain vitamin D3, which is metabolized more efficiently than D2.
In a study published last year (full citation below), the investigators compared various management practices with 25(OH)D levels across several herds. Levels of vitamin D in the cows and heifers looked pretty good: all herds had 25(OH)D averages above 30 ng/mL, which is considered the minimum for vitamin D sufficiency. However, the herd that was supplementing at only 20,000 IU/day (rather than the 30,000-50,000 IU/day of the others) did have 22% of their cows below that sufficiency threshold.
The situation for calves in this study wasn’t quite so rosy. Now, newborn calf levels of serum 25(OH)D are typically much lower than in older animals—in this study they averaged 15 ng/mL. In the six herds examined, 25% of newborn calves had serum 25(OH)D concentrations below 10 ng/mL. If left uncorrected, these calves in particular could suffer impaired health. If we look at the figure below, we see distinct differences across farms as the calves age. (We’re looking exclusively at the pre-alfalfa-eating stage here.) Spring/summer sun exposure or supplemental vitamin D in the diet would seem to make a significant difference in a calf’s vitamin D level.
Given that vitamin D is associated with growth, development, and immune function, this nutrient is required starting with a calf’s first days. Most milk replacers contain adequate vitamin D. If raising calves on milk, one should provide supplemental vitamin D3 at a rate of 6000-10,000 IU/kg of dry matter. Additionally, giving calves a 50,000-100,000 IU bolus of vitamin D3 at birth may also be helpful.
(Before initiating a new treatment or nutrition regimen, you should consult your veterinarian/nutritionist.)
Dystocia (difficulty calving) is hard on a cow, especially when the calf (or calves, blasted twins!) has to be pulled. That trauma to the reproductive tract can cause pain and inflammation that can last for several days. As we know, cows that don’t feel good often don’t spend as much time at the feed bunk, and cows that eat less than they should, make less milk than they could. When we humans feel achy, we often take an NSAID (nonsteroidal anti-inflammatory drug, like ibuprofen). Maybe we should do the same for our cows around calving?
In a study just published in the January 2017 Journal of Dairy Science, the investigators gave flunixin meglumine (Banamine®) immediately precalving and then again 18-36 hours later. As it turned out, that was a bad idea! The precalving dose was discontinued after the first week of the study (72 animals) because the treated group had 26% stillbirths vs. 5% in the control group. For the rest of the study (~1200 animals) the treatment group only received doses of flunixin at ~1 hour and ~24 hours post calving. The results: through 14 days in milk, cows treated with flunixin produced significantly less milk (3.5 lbs./day) than the untreated cows. Additionally, flunixin-treated cows had an increased likelihood of retained placenta. Bottom line: it is inadvisable to give periparturient cows flunixin meglumine (Banamine®).
So are there other NSAIDs that could help out cows after calving?
A few years ago, the same research group looked at meloxicam as a pain reliever for cows that had needed assistance calving. Animals in the treatment group received a single injection of meloxicam approximately 24 hours after calving. They found that meloxicam-treated cows had the same dry matter intake and milk production as their untreated herdmates. The treated cows did spend a little more time at the feed bunk, which may indicate that the NSAID was reducing pain.
The post-calving use of ketoprofen was explored in a study published in 2009. Each cow received a dose of ketoprofen as soon as possible after calving and then a second 24 hours later. Treated cows tended to have fewer cases of retained placenta than control cows, but the difference was quite small. Ketoprofen treatment did not result in a difference in early-lactation milk yield or subsequent fertility. So like meloxicam, ketoprofen doesn’t seem harmful (unlike flunixin), but it’s probably not particularly helpful either.
Something simpler than an NSAID?
Interestingly, an older study (1997) found that ingestion of amniotic fluid at calving seemed to have a pain-dampening effect. That study was prompted by similar findings in rats. Allowing a cow to lick her baby clean may have benefits beyond a dry and stimulated calf.
Future investigations into pain relief for calving, especially dystocia, will hopefully give us more effective options for getting our cows feeling better quickly.
(Before initiating a new treatment regimen, be sure to consult your veterinarian and observe any drug use restrictions.)