Earlier this month, a beef-type cow in Florida was identified as having bovine spongiform encephalopathy (BSE), also called mad cow disease. For those old enough to remember, BSE was the cause of death (by disease and culling) of many thousands of cattle—most heavily in the United Kingdom—in the late 1980s through early 2000s.  Worse yet, it caused the deaths of a couple hundred people who had consumed beef from infected cattle (in humans, this is called variant Creutzfeld-Jakob disease).

The “bad” prion protein (PrPSc) converts normal PrP proteins.

The caused-many-deaths BSE is referred to as classical BSE, where the route of infection was due to ingestion by cattle of the infectious agent: a nasty little misfolded protein called a prion, specifically a prion designated PrPSc. Infection with PrPSc came from affected animals that were recycled into meat and bone meal and fed to other cattle. When the molecules of PrPSc get into the body, they go around refolding the native, normal PrPC proteins into the abnormal PrPSc proteins (see figure). As the disease progresses (over years), normal brain tissue becomes decidedly abnormal, and the animal’s behavior follows suit. Key symptoms of BSE include nervousness or aggression, abnormal posture, and lack of coordination. Cattle exhibiting such behaviors are not allowed in the food chain and are automatically tested for BSE.

Due to bans on the recycling of higher-risk tissues into feed, identified cases of classical BSE have fallen to essentially zero worldwide. What surveillance programs have picked up are a very few cases of what is called atypical BSE. The prions detected in these cases are slightly different at the molecular level from that in classical BSE. Atypical BSE arises from a spontaneous mutation in the gene that encodes the native PrP protein with the result that they start to misfold into a PrPSc-like shape. Like the atypical BSE-affected cow recently identified in Florida, these cases are not caused by infection from the outside.

Discovery of this “mad” cow (and the five others over the last 28 years) demonstrates that the surveillance procedures conducted by USDA are effective. At this point, USDA is testing about 25,000 cattle a year, and those are largely sampled from older or ill animals. USDA estimates the prevalence of BSE in the US at 1 in 1 million cattle.

Bottom line: we will occasionally see cases of atypical BSE pop up due to nature (mutations happen!) and our well-functioning surveillance system, but risk to the health of people and other cattle is exceedingly low.

Additional information:

on this recent case (August 2018; USDA)

USDA’s general information on BSE

CDC’s information on BSE

Are too many heifers on your farm showing up with mastitis early in that first lactation? You may want to examine your prevention strategies. A review paper that examined the effectiveness of various precalving treatments in heifers was published earlier this summer. Here are the key take-a-ways:

developing udder on a Jersey heifer
She’ll be in the parlor soon.
photo: Spirited Rose Homestead Dairy Farm
  • When the infection is caused by contagious bacteria (e.g., Streptococcus agalactiae, Staphylococcus aureus), antibiotics, teat sealants, and vaccines can improve udder health outcomes.
  • Particularly if you are considering using antimicrobial treatments, culture quarter milk so you know who the enemy is. We want to minimize the development of antibiotic resistance.
  • When environmental pathogens (e.g., Escherichia coli, non-agalactiae streptococci) are the problem, teat sealants and combination therapies are effective at reducing mastitis risk.
  • When coagulase-negative staphs (CNS) are infecting heifer udders, antibiotics, teat-sealants, and combination therapies offer the most help.
  • When employing any of these treatment options, be sure they are delivered by a well-trained person.
  • On farms with effective fly control and that minimize stress for late-gestation heifers, there may be little benefit from preventative medical treatment.

The paper: Naqvi, Nobrega, Ronksley, & Barkema. June 2018. Effectiveness of precalving treatment on postcalving udder health in nulliparous dairy heifers: A systematic review and meta-analysis. Journal of Dairy Science 101:4707-4728.

Another good resource is the National Mastitis Council’s Heifer Mastitis Prevention and Control Plan.

Researchers from Oregon State University investigated the blood serum profiles of Holstein cows before and after calving and compared those that developed clinical mastitis with those that did not. To do so, they used ultra-performance liquid chromatography high resolution mass spectrometry plus statistics to identify differences in concentration of metabolites, lipids, minerals, and inflammatory markers in blood serum. It’s OK if you read that last sentence and went, “Huh?”  The short version is that they ran blood serum samples from dry cows through some fancy laboratory equipment to see if there were any indicators associated with developing clinical mastitis after calving. And yes, there are!

For example, alpha-tocopherol (a form of vitamin E) levels were significantly higher in the blood of cows that did not develop clinical mastitis compared to those that did (Figure 1). Another difference was in the overall profile of metabolites (molecules that participate in or are produced during metabolism); they were quite different for cows that remained healthy and those with post-calving mastitis (Figure 2).

Figure 1. Control animals (no mastitis; open bars) had significantly more alpha-tocopherol (vitamin E) in their blood than cows that developed mastitis (shaded bars). From Figure 4 from Zandkarimi et al. 2018.
The figure shows self-organizing map of metabolomic data.
Figure 2. See the starkly different profiles in serum metabolite concentration between cows that developed mastitis post-calving (CMP) and those that did not (Control)? The metabolites are grouped by metabolite family, e.g., carnitines. The more red colors indicate higher concentrations, while blue indicates lower. From Figure 5 from Zandkarimi et al. 2018.















While no dairies have liquid chromatography mass spec technology in their on-farm lab, these results may lead the way to identifying one or two highly reliable blood markers that could be easily measured on the dairy. And forewarned is forearmed, right? Knowing which cows were likely to develop mastitis could allow proactive treatment to prevent the more expensive and damaging clinical mastitis.

The paper: F. Zandkarimi, J. Vanegas, X. Fern, C.S. Maier, G. Bobe. Metabotypes with elevated protein and lipid catabolism and inflammation precede clinical mastitis in prepartal transition dairy cows. Journal of Dairy Science, June 2018, 101:5531–5548

Young Calf Health Workshops

Best Management Practices for Young Calves  (December 1, 2017, 1-4 pm)

Interventions for Sick Calves  (December 8, 2017, 1-4 pm)

Classroom and hands-on instruction at OSU in Corvallis.

For more detailed information, click to open the flier:

young calf health workshop flier 2017.12

To register, go to http://bit.ly/MarionDairyWorkshops

Cow traversing footbaths (somewhere it doesn’t rain much). Photo from Shield Agriculture.

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).

three line graphs showing normal and abnormal activity levels over a 24-hour day for cows affected by lameness or mastitis or in heat
Average activity levels of healthy, not-in-heat cows (solid lines) and “affected” cows (dashed lines) over the course of a day. Lower activity levels correspond to more resting and higher activity levels to more eating and moving around. Data from 350 cows over 5 months show that circadian patterns differ between “normal” and “affected” cows. Figure is from Veissier et al. 2017 Journal of Dairy Science 100:3969–3974.

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.

Headstone marking the grave of You’ll Do Lobelia, a purebred Jersey cow, 1932-1941
They sure don’t all get this kind of memorial. photo: slgckgc via Flickr

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.

two hornless calves on mowed grass
Hornless calves (named Buri and Spotigy) produced by gene editing. Photo from Carlson et al. 2016 Nature Biotechnology 34:479-481

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.)

Nelson et al. 2016. Vitamin D status of dairy cattle: Outcomes of current practices in the dairy industry. Journal of Dairy Science 99:10150-10160.

line graph showing blood vitamin D levels of six groups of calves across six weeks
(Modified) Figure 4 from Nelson et al. 2016. Serum 25-hydroxyvitamin D [25(OH)D] of Holstein dairy calves according to various housing and nutrition practices. Each point represents the mean and 95% CI of samples from at least 6 calves. The samples collected at 0 wk of age were collected after colostrum consumption. Open triangles (△) and dashed line represent calves from a herd in Idaho fed pasteurized waste milk with no supplemental vitamin D3 limited sun exposure (calves were housed in either hutches or barn and samples were collected in winter). Open circles (○) and dashed line represent calves from a herd in Florida fed pasteurized waste milk with no supplemental vitamin D3 and no direct sun exposure. Filled circles (●) and solid line represent calves in the same herd that received 150,000 IU of vitamin D3 at birth via injection and pasteurized milk supplement that provided 5,000 IU/d. Filled diamonds (◆) and solid line represent calves fed whole milk 3 times/d and kept outdoors in Florida (samples collected in mid-April). Filled squares (■) and solid line represent calves from a herd in Georgia fed milk replacer containing 6,600 IU/kg of DM. The calves received 0.8 kg/d of milk replacer from 0 to 14 d and 1.2 kg/d milk replacer from 15 to 42 d and raised under shade. Filled triangles (▼) and solid line represent calves from a herd in Florida kept outdoors in a group pen and fed ad libitum milk replacer containing 11,000 IU of vitamin D3/kg of DM.

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?

Photo of a Holstein cow licking her newborn calf.
Photo: Carla Wardin, Truth or Dairy

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.)