Learn cattle reproductive anatomy and physiology, heat detection, estrus synchronization, semen handling, gestational nutrition, and sire selection in the classroom and practice artificial insemination with reproductive tracts and live animals.
When: March 27-29, 2019
Where: Eastern Oregon Agricultural Research Center, Burns
Cost: $375
Class size is limited; register ASAP to secure a spot. For full details and registration information, click on the flyer link below.
Learn cattle reproductive anatomy and physiology, heat detection, semen handling, artificial insemination technique, and sire selection in the classroom and on live animals.
When: February 26-March 1, 2019
Where: Owyhee County Extension Office, Marsing, Idaho
Cost: $325 for entire school or $125 for “tune-up” session
Languages: English, Spanish
For full details and registration information, click on the flyer link below.
Topics on tap for the Central Oregon Forage Seminar (2019) include: producing low-carb horse hay, effects of storage on hay quality, the 2019 water outlook, forage pest control, measuring reduced lignin quality, and industrial hemp.
When: Wednesday, January 30, 2019 (all day)
Where: 4-H Clover Club Building, Prineville, Oregon
RSVP to OSU Crook County Extension Service (541-447-6228) by January 25.
Full details on this document: Central Oregon Forage Seminar 2019.01.30.
The Oregon Hay & Forage Association and Oregon Forage & Grassland Council are holding a Fall Forage Festival, which will include conversations about hay nutrient values and storage, coping with drought, current research, and resources. Plus the Hay King Contest!
When: November 16 and 17
Where: Corvallis, Oregon
Cost: $30 (includes lunch)
For the rest of the details, click the pdf link below.
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 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)
Educational seminars (maximizing corn silage quality, effects of drought stress on digestibility, water conservation) and free lunch(!) are at the University of Idaho Kimberly Research and Extension Center. The field day is September 13, 2018, 10:00-2:00.
For additional details and to RSVP (by September 10), click here to open the flyer.
So what’s all this business about A2 milk? How is it different from A1 milk? Is it hooey? What do these codes refer to anyway?
Starting with the last question first, A1 and A2 refer to “versions” of the beta-casein gene. In this case, the gene in question encodes the protein beta-casein, one of three casein proteins, which is, of course, a key component of cheese. The A2 version of this protein varies just a little bit in its structure from the A1 version. An individual cow’s genotype could be A1A1, A2A2, or A1A2 for the beta-casein gene; her milk would then contain whichever protein versions her genes dictate.
The a2 Milk Company claims that A2-only milk is easier on digestion. A recent study has suggested that in milk-sensitive individuals, milk containing A1 protein may be associated with symptoms of discomfort after milk consumption, and with strictly A2 milk those symptoms may be lessened. Also, gastrointestinal transit time appears to be slower with A1 milk consumption but, contrarily, yielding softer stools. Additional studies to provide replication of these findings are needed. Early studies on A1 and A2 milk that suggested a link between A1 milk and several diseases have been unsupported by subsequent investigations. That is, there is no evidence that consuming milk containing A1 protein carries any disease risk.
So, should breeding decisions be made on the basis of beta-casein genotype? Or perhaps the question is, is A2 milk a fad or a legitimate, long-term slice of the market? Does A1 vs. A2 matter for yogurt or cheese making? There is a lot we still don’t know about the biology of milk. However, there would seem to be little risk in choosing A2A2 bulls. There are quite of few of them out there, although the number varies by breed. The most comprehensive and recent documentation of beta-casein genotype by breed has been compiled by the Canadian Dairy Network (see table).
Available data from U.S. cattle are more limited in number and over 20 years old. Interestingly, Zebu- or Brahman-type cattle have a very high frequency of A2A2.
Bottom line, don’t compromise your primary genetic objectives for your herd just to chase an A2A2 genotype, but there’s likely no harm in moving that direction if it makes sense for your market of the future.
For a deeper dive into the biology of A1 and A2, read on.
A1 and A2 refer to types of gene variants of the beta-casein gene. A gene variant (an allele, for those who remember their biology) is when we have a difference in the DNA sequence for a particular gene. The A2 gene variant encodes a proline (a particular amino acid; you’ll recall that amino acids are the building blocks of proteins) at position 67 in the 209-amino acid chain that forms beta-casein (see figure below). The A1 gene variant encodes a histidine at position 67.
The A1 beta-casein protein is thought likely to be cleaved (cut) during gastrointestinal digestion at the position 67 histidine, while A2 beta-caseins are less likely to be cleaved there. Cleavage at amino acid 67 generates a short protein (a peptide) called beta-casomorphin-7 (abbreviated BCM7). BCM7 has opioid properties. Now, no need for concern. We all know that while milk is tasty, it is not a very effective painkiller nor brain manipulator. It is possible though, that BCM7 may have some effect on processes in the gut, such as slowing the rate of passage. Also, all milk contains additional types of opioid peptides. Other foods (from animals and plants) do as well.
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:
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).
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
