Sierra Foothill Research and Extension Center

Background

In 2001, the California Legislature passed the California Oak Woodland Conservation Act. This Act grew out of concern that California’s oak woodland habitats were threatened and that the State was continuing to lose oaks to development, firewood harvesting, and agricultural conversions. Such losses could critically impact a wide range of wildlife species that are so dependent on this habitat type since oak woodlands are home to more than 300 species of terrestrial vertebrates, as well thousands of invertebrates. In addition, woodlands moderate temperatures, reduce soil erosion, facilitate nutrient cycling, and sustain water quality. The Act recognized the importance of California’s oak woodlands -- how they enhance the natural and scenic beauty of this great State, the critical role of the private landowner, and the importance of private land stewardship. The Act further acknowledged how oak woodlands increase the monetary and ecological value of real property and promote ecological balance.

As a result of the Act, the Oak Woodland Conservation Program was established. This Program, administered by the Wildlife Conservation Board (WCB), is designed to provide $10 million to help local jurisdictions protect and enhance their oak woodland resources. It offers landowners, conservation organizations, and cities and counties an opportunity to obtain funding for projects designed to conserve and restore California’s oak woodlands. It authorizes the WCB to purchase oak woodland conservation easements and provide grants for land improvements and oak restoration efforts. While the Program is statewide in nature, it is designed to address oak woodland issues on a regional priority basis. Most importantly, this Program provides a mechanism to bring ranchers and conservationists together in a manner that simultaneously allows both to achieve that which is so valued -- sustainable ranch and farming operations, along with healthy oak woodlands.

The Legislature created the Oak Woodlands Conservation Program with the expressed intent to accomplish the following:

• Support and encourage voluntary, long-term private stewardship and conservation of California oak woodlands by offering landowners financial incentives to protect and promote biologically functional oak woodlands;

• Provide incentives to protect and encourage farming and ranching operations that are operated in a manner that protect and promote healthy oak woodlands;

• Provide incentives for the protection of oak trees, providing superior wildlife values on private land, and;

• Encourage planning that is consistent with oak woodland preservation.

The WCB is authorized to award cost-share incentive payments to private landowners who enter into long-term agreements. Such agreements will be structured to include management practices that benefit oak woodlands and promote the economic sustainability of the farming or ranching operations. The Act requires that at least 80 percent of the money be used for grants for the purchase of easements, for restoration activities, or for enhancement projects. In addition, the funds may be used for grants that provide cost-share incentive payments and long-term agreements.

The remaining 20 percent of the funds may be used for public education and outreach efforts by local governments, park and open space districts, resource conservation districts, and nonprofit organizations. Within this 20 percent category, funds may also be used for grants designed to provide technical assistance and to develop and implement oak conservation elements in local general plans.

In order to qualify for funding, the county or city where applicants are applying for funding from, must have an Oak Woodland Management Plan. Once the city or county has demonstrated that an Oak Woodland Management Plan exists, landowners are eligible to participate in the Program.

The Oak Woodlands Management Plan

The Act requires that Plans include a description of all native oak species located within the County’s or city’s jurisdiction. To assist with the preparation of the Plan, the Act allows nonprofit organizations, park or open space districts, resources conservation districts, or other local government entities to apply to the Wildlife Conservation Board for funds to develop an Oak Woodlands Management Plan for a county or city. However, the county or city shall maintain ultimate authority to approve the Oak Woodlands Management Plan. If two or more entities seek grant funding from the WCB to prepare an Oak Woodlands Management Plan for the same jurisdiction, the county or city shall designate which entity shall lead the efforts to prepare the necessary document.

To participate in the Oak Woodlands Conservation Program, a county or city shall adopt an Oak Woodlands Management Plan in the form of a Resolution. The Resolution does not have to be part of the General Plan. If a county or city currently has a plan in place that meets the minimum requirements of the Oak Woodlands Management Plan, a resolution by the governing body certifying such compliance is sufficient.

The Resolution adopted by the local jurisdiction shall contain at least the following elements:

• The county or city agrees to adopt a Resolution to offer private landowners the opportunity to participate in the Oak Woodlands Conservation Program. The Oak Woodlands Management Plan and Resolution is adopted pursuant to the requirements of California Fish and Game Code Section 1366 (a). Previously adopted resolutions are acceptable if they meet the minimum requirements of the Resolution.

• The county or city shall prepare statements that describe the status of oak woodlands in their jurisdiction. Such statements shall include a description of all native oak species, estimates of the current and historical distribution of oak woodlands, existing threats, status of natural regeneration and growth trends. To the extent possible, local jurisdictions shall prepare maps displaying the current distribution of oak woodlands.

• The county or city shall prepare statements recognizing the economic value of oak woodlands to landowners and the community at large. These statements shall encourages and support farming, ranching, and grazing operations that are compatible with oak woodland conservation.

• The county or city shall prepare statements recognizing the natural resource values of oak woodlands, including the critical role oak woodlands play relative to the health and function of local watersheds, soil and water retention, wildlife habitat, open space, and the reproduction or reduction of fuel loads.

• The county or city shall prepare statements recognizing that the loss of oak woodlands has serious effects on wildlife habitat, retention of soil and water and that planning decisions for oak woodlands should take into account potential effects of fragmentation of oak woodlands.

• The county or city shall prepare statements expressing support for landowners that participate in the Oak Woodlands Conservation Program. To qualify for funding consideration by the Wildlife Conservation Board, the county or city agree, pursuant to Section 1366 (f) of the Act, to certify that individual proposals are consistent with the county or city Oak Woodlands Management Plan.

• The county or city shall prepare statements that support and encourage education and outreach efforts designed to demonstrate the economic, social, and ecological values associated with oak woodlands.

• The county or city shall review and update as necessary, the Oak Woodlands Management Plan.

Eligible Participants

The Oak Woodlands Conservation Program is designed to consider grant proposals from the following participants: private landowners, local government entities, park and open space districts, resource conservation districts, and nonprofit organizations. Participants are encouraged to develop partnerships with interested individuals or organizations that are designed to leverage available technical and financial resources.

In addition, the county or city shall certify that proposed grant requests are consistent with the Oak Woodlands Management Plan of the county or city. As such, eligible participants must consult with the local county or city and obtain a certification that the proposal is consistent.

Applicants are encouraged to seek input from the local Fish and Game Biologist or other resource professionals when developing proposals that request funding for conservation easements, development of management plans, or long-term agreements. To learn more about this Program, or to download an application package, please visit the WCB web site at http://www.dfg.ca.gov/wcb/, or contact Marilyn Cundiff, the Program Administrator, at email: MCundiff@dfg.ca.gov., or phone: (916) 445-1079.

Introduction

Low rates of return on investment for livestock operations are a fact of life. Producers have little impact on the market price for their cattle; therefore management must be focused on the things producers can actually do something about. For many years, genetic selection programs have focused on production (output) traits, with little attention given to production costs (inputs). Recently, this view has begun to change, and the efficiency of conversion of feed (i.e., the amount of product per unit of feed input) has been recognized as more important. Numerous studies have shown what cattlemen have always known: profitability in this business depends on keeping the costs of production to a minimum. Within any beef cattle operation, feed costs are undoubtedly the main concern, since they typically account for 60 – 65 % of the total costs of production. That’s why greater feed efficiency has been targeted as a means of improving the profitability of the beef industry.

One estimate of feed efficiency is the feed conversion ratio. Traditionally, this was expressed as a feed:gain ratio, but this led to the confusing result that a higher ratio meant a lower efficiency. Today, feed conversions are often expressed as a gain:feed ratio to overcome this problem. Even so, results can be misleading, because these ratios are closely correlated to the intake and rate of gain of the animal (Carstens et al., 2004). So, two animals might have similar gain:feed and still be very different in their feed intakes and rates of gain. Conversely, the same animal at different intakes would certainly have different gain:feed ratios, even though the genetics of the animal hadn’t changed. Therefore, gain:feed has never taken off as a criterion for genetic selection.

Residual feed intake (RFI), defined as actual feed intake minus the expected feed intake of each animal, was first proposed as an alternate measure of feed efficiency by Koch et al. (1963). It can be defined, in other words, as the difference between actual feed intake and the expected feed requirements for maintenance of body weight and for weight gain. RFI has been adopted more intensively in other countries, such as Australia and Canada, but in the US more attention has been given to understand the biological issues around this concept. Genetic selection to reduce RFI can result in progeny that eat less without sacrificing growth performance (Herd et al. 1997; Richardson et al. 1998). In contrast to gain:feed, residual feed intake is independent of growth and maturity patterns. Therefore, RFI should be a more sensitive and precise measurement of feed utilization, since it is based on energy intake and energy requirements. Methodology for measuring RFI

The residual feed intake is an individual record, taken in long term feeding trials (at least 70 to 84 days) where animals are housed either in individual or group pens, and accurate measurements are made of daily feed offered and refused, as well as average daily gain. Research has shown that there is considerable individual animal variation in feed intake above and below that expected or predicted on the basis of size and growth. That statement, along with the fact that individuals of the same body weight require rather widely different amounts of feed for the same level of production establishes the scientific base for measuring RFI in beef cattle.

In order to obtain RFI values, it is necessary to measure and record the daily feed intake for each animal, which can be accomplished by housing them in individual pens. Recent techniques employing electronic devices that identify each animal individually, opening specific feed bunks and measuring the feed intakes of individual animals kept in groups can also be adopted, although some difference has been observed when comparing these two types of housing. Therefore, obtaining RFI data is laborious and expensive, and this has limited its spread as a feed efficiency measurement.

Figure 1. Actual and predicted dry matter (DM) intakes by fed steers. Residual feed intake (RFI) is the difference between actual and predicted DM intakes.

Once the trial is finished, the daily feed intake is calculated from the amounts of feed offered and refused, and the average daily gain and average body weight obtained for the same period. The expected feed (or dry matter) intake is obtained from linear regression of DMI on mid-test BW.75 and average daily gain (ADG). The statistical model is: Y = β0 + β1 X1 + β2 X2 + ε where Y is expected dry matter intake, β0 is the equation intercept, β1 and β2 are the coefficients of the equation, X1 is the mid-test metabolic body weight, X2 is the average daily gain, and ε is the residual. The intercept of the equation is tested and if it is not significant a new equation is fitted without the intercept. Then, the predicted feed intake of each animal is estimated using the equation. This prediction may be thought of as the “average” or expected value for animals of similar weights and rates of gain. The actual feed intake minus the predicted feed intake corresponds to the residual feed intake (Figure 1).

Results and Discussion

Figure 2 shows the relationship between dry matter intake and average daily gain, obtained from 36 animals in a recent trial conducted at the UC Davis feedlot. These data show the general trend for increasing rates of gain with higher intakes, and also the variation around that trend. For example, two animals with identical intakes (7.43 kg) had more than 50% difference in average daily gain! Clearly, the more efficient animal would be much more profitable. Similarly, two animals with almost identical rates of gain (1.5 kg/day) had very different feed intakes (7.43 vs. 9.22 kg/day). Obviously, the animal with the same rate of gain and lower feed intake would be far more profitable.

Figure 2. Relationship between dry matter intake and average daily gain in fed steers

For a trait to be used as a selection criterion it must present genetic variance and be heritable. Several studies have shown heritabilities for RFI ranging from 0.14 to 0.44 and genetic variances ranging from 0.149 to 0.267 (Fan et al., 1995; Archer et al., 1997; Arthur et al., 2001; Herd et al., 2003). From a practical point of view, this means that RFI is at least as heritable as early growth. The genetic variance is limited, but it is still enough to make substantial improvement. In that sense the development of an EPD for RFI seems practical. As observed by Herd et al. (2003), selection against postweaning RFI in heifers has the potential to lead to a decrease in feed intake and improvement in feed efficiency of the breeding herd, since the correlation between post-weaning RFI and cow RFI is very high (0.98). This means that selection for lower RFI in growing animals will result in lower RFI in breeding females, thereby reducing the feed cost for the cow herd. Conclusions Profitability depends on keeping costs to a minimum without sacrificing production or quality. Feed represents about 2/3 of costs of beef production, so more efficient conversion of feed should be a priority. Residual feed intake is the best available measure of efficiency, because it is independent of level of production; moreover, RFI is moderately to highly heritable, and so will respond to genetic selection. Selection for reduced RFI in growing animals should reduce feed costs for beef cattle in all stages of life, including the cow herd.

Literature Cited

Archer, J.A., Arthur, P.F., Herd, R.M., Parnell, P.F., Pitchford, W.S. 1997. Optimum postweaning test for measurement of growth rate, feed intake, and feed efficiency in British breed cattle. J. Anim. Sci., 75:2024-2032. Arthur, P.F., Archer, J.A., Johnston, D.J., Herd, R.M., Richardson, E.C., Parnell, P.F. 2001. Genetic and phenotypic variance and covariance components for feed intake, feed efficiency, and other postweaning traits in Angus cattle. J. Anim. Sci.79:2805-2811. Carstens, G., Welsh, T., Randel, R., Holloway, B., Forrest, D., Keisler, D. 2003. Residual feed intake studies in growing steers and bulls. In WCC-92 Beef Cattle Energetic Station Report, Reno, Nevada. Fan, L.Q., Bailey, D.R.C., Shannon, N.H. 1995. Genetic parameter estimation of postweaning gain, feed intake, and feed efficiency for Hereford and Angus bulls fed two different diets. J. Anim. Sci. 73:365-372. Herd, R.M., Archer, J.A., Arthur, P.F. 2003. Reducing the cost of beef production through genetic improvement in residual feed intake: Opportunity and challenges to application. J. Anim. Sci. 81 (E. Suppl. 1): E9-E17. Herd, R.M., Arthur, P.F., Archer, J.A., Richardson, E.C., Wright, J.H., Dibley, K.C.P., Burton, D.A. 1997. Performance of progeny of high vs. low net feed conversion efficiency cattle. Proc. 12th Conf. Assoc. Advancement Anim. Breed. Genet, Dubbo, Australia. Pages 742-745. Koch, R.M., Swiger, L.A., Chambers, D., Gregory, K.E. 1963. Efficiency of feed use in beef cattle. J. Anim. Sci. 22:486-494. Richardson, E.C., Herd, R.M., Archer, J.A., Woodgate, R.T., Arthur, P.F. 1998. Steers bred for improved net feed efficiency eat less for the same feedlot performance. Anim. Prod. Aust. 22:213-216.

Over the past four months we have read and heard more about BSE (Bovine Spongiform Encephalopathy; Mad Cow Disease) than we may have ever wanted to know. The California Cattlemen’s Association and other allied groups, particularly the NCBA have done a wonderful job in terms of getting out the facts about BSE and the message that beef is safe for consumers. The BSE issue is extremely complicated and I will compare some of what has been done in France with our situation in California.

What are the critical control points for preventing BSE in U.S. cattle?

The first step is to prevent the introduction of cattle into the U.S. that might be “incubating” the disease. This is the basis of our ban on the importation of any cattle from countries that are known or suspected of having BSE. For example, we banned the importation of cattle from Britain after 1986 and banned live cattle importation from Canada in May of 2003. Secondly, because this disease is transmitted by the feeding of contaminated meat and bone meal (MBM), the feed ban on feeding ruminant MBM to cattle was put into effect in 1997 in the U.S. Obviously, it is imperative that this feed ban be strictly enforced and this is the responsibility of the Food & Drug Administration (FDA). The third measure is to have an active surveillance program to be sure the other preventive measures are working correctly. The surveillance program must include potential clinical cases of BSE and must also include “at-risk cattle” (downer cattle are part of this “at-risk” group). Additionally, our veterinary diagnostic laboratories are excellent at detecting various diseases in cattle, especially diseases like BSE or rabies that have public health concerns. The monitoring of clinical cases of BSE has been actively occurring for almost 18 years. Secondly, the surveillance of “at-risk cattle” has also been an active area for a number of years. This is the part of the surveillance program that found the BSE-positive Canadian dairy cow in Washington state last year. In 2003, the USDA tested about 20,000 cattle for BSE. The USDA’s surveillance of “at-risk cattle” had focused on downer cattle at slaughter houses. Because downer cattle can no longer be slaughtered for human consumption, the USDA will need to accomplish this part of the surveillance program by other methods. It is still extremely important to monitor this group of animals for BSE. In March, 2004 the USDA announced that BSE testing will be done on 286,000 or more cattle per year for the near future. Also, this testing will be accomplished by using the agency’s network of 20 regional laboratories and by the use of the rapid test technology that allows negative results to be reported within 24 hours or less. Additionally, to satisfy our export markets (Japan, South Korea, etc); it may become necessary to test a percentage of healthy cattle over 30 months of age when they are slaughtered. Therefore, surveillance of cattle for BSE will continue to be an important part of our preventive measures. An additional preventive measure in the future will be the development of cost effective tests that can be used on live animals. This would allow us to detect BSE “infected” cattle before slaughter. Sheep also have a transmissible spongiform encephalopathy called Scrapie and there is a test to detect this disease in the live animal. Also, some sheep are resistant to Scrapie and some are more susceptible. Currently, there are genetic tests available to detect this resistance or susceptibility. To prevent BSE it would be extremely helpful to have both live cattle tests and genetic susceptibility tests. Hopefully, these tests can be developed and implemented in the future.

What are the critical control points for food safety with regard to BSE?

The main food safety procedure is to prevent BSE in U.S. cattle in the first place. If healthy slaughtered cattle over 30 months of age are tested for BSE it is essential to have “test and hold” facilities at the plants. The carcasses will have to be held until the negative test results are reported. This would prevent the possibility of large scale meat recalls due to false positives. A very important procedure is to eliminate the “specified risk materials” (SRMs) from the human food chain. This process has already been initiated. The SRMs include the brain, eyes, skull, tonsils, spinal cord, spleen, small intestines, vertebral column (bones of the neck and back that surround the spinal canal), and thymus. For animals over 30 months of age, the SRMs will be removed from the carcass, segregated, and eliminated from the food supply.

How does France compare to California? Both have very large agricultural bases. France is about 1.3 times the size of California. France has a population of 60 million and California has about 36 million people. If we count all the beef cattle, calves, dairy cattle, stockers, and feedlot cattle in California the number is probably less than 6 million, in France there are 20 million cattle. The average herd size in France is about 70 head and the average farm size is 140 acres. France is first in beef exports in the European Union (EU) and California is number one in agricultural exports in the U.S. France diagnosed their first case of BSE in 1991 and has had about 900 confirmed cases since that time. We have not seen a case of BSE in California and the U.S. has only had the one BSE case imported from Canada. What does the BSE prevention program in France look like?

Many of the points covered in the first section are included in the French program. Their ban on feeding meat and bone meal started in 1990 and has been expanded several times in subsequent years. Currently, meat and bone meal from any source cannot be fed to any farmed animals (including poultry, swine, or sheep) in France. The ban on meat and bone meal feeding is the most important preventive measure in BSE control programs. The surveillance program in France was also started in 1990 and focused on clinically sick cattle that might have BSE. In the year 2000, they begin to look at all “at risk cattle” and are currently testing over 270,000 cattle in this category per year. Additionally, beginning in 2001 all healthy cattle over 24 months of age at slaughter are tested. The number of cattle in this last category is 3 million per year. Since 1991, there have been just less than 900 cases of BSE diagnosed in France. Twenty-three percent (23%) of these have been in clinical cases, 47% have been in “at risk cattle”, and 30% have been in healthy slaughtered cattle. Additionally, the majority of BSE cases diagnosed were born after the 1990 feed ban. This is a very important point we need to remember.

What does the BSE prevention program in France cost?

During 2003 the French program for BSE prevention and surveillance cost them about 900 million dollars (750 million Euros). This amount was about 57% of the total animal health budget for France. Much of this cost is for the removal and disposal of the SRMs from slaughtered animals. Additionally, the animal identification program needed to track the animals from their farm of origin through slaughter is another cost to be considered.

Does BSE occur spontaneously in cattle?

The message that BSE occurs spontaneously in cattle has been repeated in the media several times. Where does this idea come from? There is a disease in humans called Creutzfeldt-Jakob Disease (CJD) which does occur spontaneously. It occurs at a rate of about 1-2 people per million population per year, worldwide. This is the so-called spontaneous CJD. Some have extrapolated this information to the cattle population, saying that BSE occurs spontaneously in cattle just as spontaneous CJD occurs in humans. Therefore, if we have about 100 million cattle in the U.S., we have 100-200 cases of BSE each year. This assumption is the basis for the argument that we should be testing every slaughtered animal for BSE. There is no basis in fact for this assumption, however. To the contrary, there is ample evidence that BSE is not occurring spontaneously. For example, we have been able to detect cattle diseases with public health significance that occurs at a much lower rate than 1 per million and one such disease is rabies. The diagnosis of rabies is dependent on a thorough examination of the brain of the animal. BSE diagnosis is also dependent on the complete examination and testing of the animal’s brain. In California, cattle rabies is detected every year or so and almost every case is associated with significant human exposure. If we were unable to detect this central nervous system disease (rabies) one or more fatal cases of rabies in humans would occur. The fact is, we are able to routinely diagnose rabies and the same experts are more than capable of diagnosing BSE. Every veterinary diagnostic laboratory in every state is actively looking for BSE and has been since 1986. We are not missing the diagnosis of BSE in cattle in the U.S. Those who are publicly concerned about spontaneous BSE in cattle and who advocate testing all slaughtered cattle are not at all concerned about beef products imported into the U.S. If BSE does spontaneously occur, it must do so world wide, thus imported beef products would carry the same or greater risk. We must insist on using the science as our guide in making policy regarding BSE.

Research similar efforts in other regions

Research was completed on similar efforts in other regions. There are over 300 grass-fed beef marketing operations across the United States. Here in California, there are approximately 10. Most are selling approximately 50-60 head per year. This appears to be a marketing limit for those who produce, process, market and distribute on their own. Additional labor and space requirements for marketing, storage for dry-aging, and distribution appear to be the biggest barriers to increasing market share for producers working individually.

The largest grass-fed beef company in California is marketing around 1,000 head annually primarily to Bay Area restaurants. Branded beef consultant Allen Williams has noted the grass-fed beef market still has plenty of room to expand and that price is not a limiting factor. Ervin’s Beef in Arizona has noted that you can market all you can produce. One Bay Area restaurant is wanting grass-fed beef and is willing to work with other restaurants and independent retail outlets to help move the entire carcass and insure the company they are working with will be able to grow large enough to insure they stay a viable business.

Producer Survey Results

Based on a response rate of 27 percent (out of 466 surveys mailed), there is adequate supply to initially meat market demand. On average, ranchers in the HSB project area have 30 years of ranching experience. The average age of ranchers in the project area reflects statewide trends, with 79.1 percent of the respondents being over 45 years of age (opposed to only 5.6 percent under the age of 35). Most producers (81.7 percent) are in the cow-calf business, while seedstock producers (24.6 percent), stocker operators (17.5 percent) and feedlots (4.8 percent) are also represented. Most producers use English breeds – 67 percent of the bulls owned by those who responded were Angus. Cows were predominately Angus and Hereford.

Total cattle numbers for survey respondents are summarized below:

Class Total Average Bulls 663 7.1 Cows 11,327 106.9 Heifers 3,578 37.3 Steers 2,374 32.5

Seasonal supply of cattle does not appear to be a problem as shown in the following table, which reflects number of cattle sold per season by respondents:

Class Spring Summer Fall Winter Cows 204 338 840 230 Heifers 706 1662 279 728 Steers 665 1755 909 739 Bulls 36 36 100 67

More than 40 percent of respondents have participated in quality assurance programs, and nearly 55 percent keep herd health records. Only 5.6 percent indicated that they feed antibiotics to their cattle, and just 10.3 percent use implants. These elements may become critical in marketing a niche product.

Those who responded run cattle on 84,695 acres of owned land and 63,847 acres of leased land. Respondents include small, medium and large producers. Many are involved in conservation programs, as well; this could be used as a marketing message (see the table below):

Program No of Ranches Acreage Williamson Act 54 50,955 Super Williamson Act 2 6,350 Environmental Quality Incentives Prog 7 6,350 Wildlife Habitat Incentives Program 2 250 Conservation Easements 11 21,213

Consumer, Restaurant and Retail Surveys Three product samplings were conducted with 700 consumers at events in Placer and Nevada counties. During the samplings, surveys were distributed. Survey respondents ranked the same beef attributes on the same 5 point scale as the restaurant and store market survey conducted in March 2003. A total of 142 surveys were returned. The restaurant and market surveys were conducted with 29 establishments in the six-county area.

Results from the consumer surveys and how they compared with the March 2003 survey were as follows (1 = not at all important and 5= very important):

Attributes Consumer Avg Restaurant and Retail Store Avg Flavor 4.7 4.7 Tenderness 4.7 4.7 Food Safety Assurances 4.7 4.8 Quality Assurance Certified 4.7 4.1 Consistent Quality 4.6 4.9 Nutritional Value 4.6 3.6 Antibiotic Free 4.4 3.7 Hormone Free 4.4 3.7 Dry Aged (14 to 21 Days) 4.3 3.3 Locally Produced On a Family Ranch 4.0 3.2 Grass-fed 4.0 2.8 Recipes & Other Product Information 3.5 2.4 Breed 3.3 3

Most of the establishments surveyed purchase a range of beef products, from steaks and roasts to ground beef. Nearly all of the establishments expressed an interest in participating in product taste testing with HSB.

Results from the consumer surveys were similar in some aspects with the March 2003 Restaurant and Retail Store survey. Both surveys were in agreement on the top 5 attributes, although not in the same exact order. These attributes were:

1. Consistent Quality 2. Food Safety Assurances 3. Flavor 4. Tenderness 5. Quality Assurance Certified

Consumers also placed a higher score on nutritional value, antibiotic-free, hormone-free, dry-aged, locally produced, and grass-fed. Anecdotal comments from the product samplings seemed to indicate that locally grown and grass-fed are important. Interviews with two Bay area restaurants indicate that grass-fed and locally grown are important marketing attributes.

Processing Results

High Sierra Beef purchased a five-year old cow and a two-year old heifer. These were processed at Johansen’s Meat in August. The cow’s carcass weights yielded 897 pounds for the cow and 512 pounds for the heifer. The majority of the meat was ground into hamburger. The tenderloins and tri-tip was pulled from both carcasses to sample some premium cuts of beef. The ribeye on the heifer was also pulled.

The cow’s fat was yellow due to her age and time grazing on irrigated pasture and annual rangeland. The heifer’s fat was more of a cream color due to her younger age. The ground beef from the cow was formulated into 13% fat. To test value-added opportunities, 50 pounds of the cow was made into a beef stick. The yield on the beef stick was 33 pounds.

Current Work

High Sierra Beef is currently working on completing a financial model and selecting a business model. Work is continuing on finalizing protocols and grazing strategies to ensure a consistent product. The Executive Committee will review business plan development in May to determine whether to proceed with forming a business. If that decision is affirmative, product testing and development would occur throughout the summer and fall of 2004. Product would be available to sell in spring 2005.

Bovine virus diarrhea (BVD) is a complicated disease to discuss as it can result in a wide variety of disease problems from very mild to very severe. BVD can be one of the most devastating diseases cattle encounter and one of the hardest to get rid of when it attacks a herd. The viruses that cause BVD have been grouped into two genotypes, Type I and Type II. The disease syndrome caused by the two genotypes is basically the same, however disease caused by Type II infection is often more severe. The various disease syndromes noted in cattle infected with BVD virus are mainly attributed to the age of the animal when it became infected and to certain characteristics of the virus involved.

Diseases caused by BVD infection

Fetal BVD infections (infection of the unborn calf): The result of a fetal infection with the BVD virus is usually determined by the age of the fetus at the time of infection. The virus is capable of passing from an infected cow to the unborn fetus which is particularly vulnerable to the BVD virus during the first 6 months of pregnancy. Death of the fetus is common if the infection occurs during the first 120 days of pregnancy and the cow will lose the pregnancy. However, if the fetus survives an early infection, it will be born without a detectable antibody titer and be persistently infected (PI) with the BVD virus. During the first 120 days of gestation, the fetus has an underdeveloped immune system and does not recognize the BVD virus as foreign. The fetus does not mount an immune response against the virus, remains infected, and does not have a detectable anti-BVD titer. It is not uncommon for the surviving fetus to be malformed; blindness, skeletal abnormalities and under-developed brains are common defects noted in such calves. A BVD PI calf may appear normal, be weak at birth, grow poorly, be susceptible to respiratory diseases, and die before they can be weaned. They may also grow normally, reach breeding age, and produce more persistently BVD infected calves (The virus is passed from generation to generation). PI carriers can only be created by infection with BVD virus during the first 110-120 days of pregnancy. These animals shed billions of virus particles every day in their urine, feces, and saliva, and are a source of infection for other animals in the herd. If the fetus becomes infected after 120 days of pregnancy, there may be an abortion but usually, because this aged fetus has a more developed immune system and can elicit an immune response against the BVD virus, a healthy calf is born that has a good level of BVD antibody titer.

Subclinical BVD infections: Most animals that become infected with BVD never show signs of disease caused by the virus; however infection can lower the animal’s resistance to other infections, which could result in illness. For example, in feedlot calves, BVD infection may go unnoticed, but the lungs become susceptible to infection with bacteria such as Mannheimia haemolytica (previously called Pasteurella haemolytica) and other agents that cause “shipping fever”. Some people believe that BVD is one of the most significant disease organisms involved with respiratory disease of cattle. Severe acute BVD infections: This disease syndrome is usually (but not always) associated with Type II BVD virus infection. The affected animals will exhibit high fevers (107-110 F), occasional diarrhea, respiratory disease, and they will not eat. Peracute BVD can affect cattle of all ages and often results in death of the animal within 48 hours of disease onset regardless of age.

Acute BVD infections: The classic, acute form of BVD is characterized by a fever of 104-106 F, discharge from the nose and eyes, erosions of the muzzle and in the mouth, and diarrhea that may contain mucus and blood. Diarrhea is usually present in every herd that has an outbreak of acute BVD, but diarrhea is not present in every animal that has acute BVD. The percentage of the herd exhibiting clinical disease and dying can vary extremely; however, if "secondary infections" are controlled, most animals survive the acute disease. This syndrome usually occurs in cattle 6 to 24 months of age. Acute Mucosal disease: An animal persistently infected with BVD virus is not able to mount any defense against becoming subsequently infected with a different BVD virus. When a BVD infection is superimposed on a PI animal, mucosal disease usually results. Acute mucosal disease is characterized by fever, profuse, watery diarrhea, erosions of the mouth, lack of appetite, discharge from the eyes and nose, and occasionally lameness. Secondary infections, such as pneumonia and mastitis, are common. Cattle with acute mucosal disease usually die within 3 to 10 days.

Chronic Mucosal disease: Some cattle that develop mucosal disease do not die as soon as expected but rather become chronically infected. Cattle with chronic mucosal disease are poor doers, and may have persistently loose stools or intermittent diarrhea, chronic bloat, decreased appetite, weight loss, erosions between the claws, or non-healing skin lesions. Discharge from the eyes and nose, bald spots due to loss of hair, and long-term lameness are also common. Cattle with chronic mucosal disease rarely survive beyond 18 months and ultimately die.

Treatment and Prevention of BVD infections There is no effective treatment for infection with BVD, but most cases are subclinical and self-limiting. Antibiotics, fluid and supportive therapy may be indicated to control secondary infections. Offering highly palatable feed could tempt sick animals to eat needed nutrients. Vaccination of susceptible cattle has been the principal approach to the prevention and control of BVD. However, preventing the introduction of BVD into your herd and identifying and eliminating PI animals from your herd are important steps to take to control the disease.

Vaccinate calves: Calves should be vaccinated twice with a modified live virus (MLV) vaccine before leaving the herd of origin. Ideally, BVD vaccinations should be completed in the calves at least 30 days prior to weaning, but whatever program you initiate needs to fit with your management system. Check with your veterinarian for specific recommendations for your herd.

Vaccinate the cow herd: It is difficult to provide blanket recommendations for vaccinating the cow herd, but some general guidelines can be given. Unvaccinated heifers and cows should be properly vaccinated before breeding to ensure protection for the fetus. All bulls should be properly vaccinated before putting them out with the cows or heifers and new additions should be properly vaccinated before adding them to the herd. Modified live virus vaccines can be safely used in open cows (there are new MLV vaccines safe for pregnant cows if the cows have been previously vaccinated with certain products) and provide long-lasting protection. Killed vaccines are safe for all cattle, but usually don’t provide as strong an immune response and may need more frequent booster vaccinations. Again, check with your veterinarian for specific recommendations.

Prevent introduction of BVD into your herd: BVD virus is shed from cattle in the feces and in secretions from the nose and mouth. BVD is also readily transmitted by aerosol droplets and direct contact. Avoiding contact with other cattle is therefore an important step to take to prevent infection from entering your herd. “Good fences make good neighbors”. It is especially important to keep pregnant cows less than 120 days pregnant separated from other cattle. New introductions into your herd need to be tested for PI status.

Eliminate PI animals from your herd: Until recently, testing cattle for PI infection was prohibitively expensive but now there are tools available making it feasible to test for and eliminate these “typhoid Mary” animals from the herd. There are two types of test available, one using a skin sample and one using a blood sample: Immunohistochemistry – for this test, a small notch of skin is taken from the edge of the ear, easily done using a pig ear-notching tool. The triangular piece of skin removed should be ¼ to ½ inches per side. Depending on the laboratory the sample will be sent to, the removed skin is placed either in a vial containing formalin or an individual plastic bag. All samples must be clearly labeled with the animals’ identification number. PCR – this test requires that a blood sample in a “purple top” tube be taken and submitted. Again, all samples must be clearly labeled with the individual animal ID.

Samples can be sent to a number of different laboratories; three are listed below. Be sure to contact the lab and talk to your veterinarian before taking and sending samples – if you take the wrong samples, all your work may be wasted. Be aware that it is possible to have “false positive” results – some animals may test positive when they are not truly persistently infected, and may need to be re-tested. Your veterinarian can help interpret the results of the testing. (Thank you to Dr. John Maas for the following information) 1. Tulare branch of the California Animal Health & Food Safety Laboratory (CAHFS)

CAHFS-Tulare Phone (559) 688-7543 18830 Road 112 Fax (559) 686-4231 Tulare, CA 93274

Sample description: Ear notch (triangle notch ¼ to ½ inch per side) in zip lock bag (or whirl pack bag). Refrigerated—not frozen. Ship overnight (not for Saturday arrival). Technique: Immunohistochemistry. Cost: $16.50 per 1-5 samples, i.e. $33.00 for ten (10) samples and $33.00 for 6 samples. Additional one time accession fee is also charged.

2. University of Nebraska, Lincoln, NE

Veterinary Diagnostic Center University of Nebraska Fair Street and East Campus Loop P.O. Box 82646 Lincoln, NE 68501-2646 Phone (402) 472-1434 Fax (402) 472-3094

Sample description: Ear notch (triangle notch ¼ to ½ inch per side) in neutral-buffered formalin. Leak proof tubes are mandatory for containers. Do not hold skin samples in formalin for more than 7 days prior to submission. Technique: Immunohistochemistry. Cost: Accession fee: $7.00 per each shipment (submission). First sample: $12.00. Two (2) to 6 samples: $20.00, multiples of 6: $20.00/six samples.

3. Davis branch of CAHFS.

CAHFS-Davis University of California, Davis West Health Sciences Drive Davis, CA Phone (530) 752-7578 Fax (530) 752-6253

Sample description: whole blood, refrigerated (not frozen). Ship in leak proof containers on ice bags (gel bags). Technique: PCR. Cost: $22.70 for the first sample, $5.65 per each sample after the first. Additional one time accession fee is also charged.

DNA (deoxyribonucleic acid) is a molecule that is shaped like a double helix and made up of pairs of nucleotides. DNA transmits genetic information. DNA is packaged into chromosomes which are located within the nucleus of all cells. Every cell in the body contains all of the chromosomes that collectively make up the genome of that organism. DNA codes for amino acids which are linked together to make proteins. A gene is a stretch of DNA that specifies all of the amino acids that make up a single protein. Proteins are the building blocks of life. There are thousands of proteins in the body (encoded by thousands of genes). The interaction and structure of proteins determines the visible characteristics or phenotype of an organism, while the genotype refers to the genetic makeup.

The sequence of nucleotides that encode a gene can differ between individuals. These differences are called genetic variants. As a result of these nucleotide differences, genetic variants or alleles may differ in the amino acid sequence of the protein they encode, or they may regulate the production of different quantities of the encoded protein. These differences can have an effect on phenotype.

All individuals receive one copy (allele) of each gene from their mother, and one from their father. The DNA sequence of a gene inherited from each parent may be identical in which case the individual is said to be homozygous for that gene, or the sequence of a gene inherited from each parent may vary in which case the individual is said to be heterozygous. Genetic variants often differ from each other by the sequence of a single base pair. These differences are called single nucleotide polymorphisms SNPs (pronounced “snips”). Genotyping means using laboratory methods to determine the sequence of nucleotides in the DNA from an individual, usually at one particular gene or piece of a gene. SNPs are commonly the basis of genotyping tests. Genetic tests based on SNPs analyze DNA derived from an individual to determine the genetic variants that are present at one specific location (nucleotide pair) in the midst of the approximately 3 billion nucleotide pairs that make up the genome.

Historically we have not known which genes contribute to performance characteristics (traits), and so we have used performance records and EPDs (expected progeny differences) to infer the genetic merit of animals. This method has been very successful at improving certain traits. Research has shown that some genetic variants of specific genes are associated in a positive way with a given trait. It is therefore possible to genotype an animal using a DNA-based genotyping test and select individuals carrying the preferred genetic variant. Marker-assisted selection is the process of using the results of DNA testing to assist in the selection of individuals to become parents in the next generation. The word “assisted” implies that the selection is also influenced by other sources of information, such as animal’s observed performance and EPDs. The genotypic information provided by DNA testing should help to improve the accuracy of selection and increase the rate of genetic progress by identifying animals carrying desirable genetic variants for a given trait at an earlier age.

It is not known which specific genes contribute to an EPD – the genes are anonymous. Complex traits, including most of the economically relevant traits for cattle production (birth weight, weaning weight, growth, reproduction, milk production, carcass quality) are controlled by many genes, and they are also greatly affected by the environment (e.g. feed conditions). Although complex traits are influenced by a number of genes – each one of these genes is still inherited in the same way. An animal inherits one copy of each gene from its sire, and one copy of each gene from its dam. These copies may differ from each other, and these differences may have either a positive or negative effect on the trait that the gene controls or influences. When an animal has a positive EPD for a certain trait, what that is effectively saying is that based on its pedigree and phenotype, it has inherited a greater than average number of “good” genetic variants of each gene affecting that particular trait.

It is important to combine DNA results (which look at single genes) with other criteria, such as EPDs (which look at numerous genes) and the animal’s actual phenotype for the trait (if available), to ensure that selection is distributed over all the genes that contribute towards the trait of interest. Don’t ignore animals that have good EPDs for a given trait and yet are not carrying the favorable form of a gene for that trait. These animals are likely to be a source of good alleles for the many other genes that contribute towards that trait. Ideally the information from genetic tests should be integrated into a genetic evaluation system that weighs all the information about an animal. Combining information from both EPDs and genetic tests into a selection decision will be superior to selection on either EPDs or markers alone. The challenge will be to determine the weight that should be given to the marker information in this decision-making process. The magnitude of the effect of a genetic variant of a gene on the trait may vary among the different breeds, production systems and environments.

INTRODUCTION

Over 20 years ago, research was underway to develop methods for in vitro fertilization utilizing bovine sperm and eggs. Freshly ejaculated sperm cannot fertilize an egg. Those sperm must reside in the female reproductive tract for 6-8 h and become diluted from seminal fluid. That process is called capacitation because it allows sperm to acquire the “capacity” to fertilize an egg. The final change sperm cells undergo after capacitation involves a morphological remodeling with release of enzymes packaged in the tip of the sperm head’s acrosome. This irreversible remodeling is known as the acrosome reaction. All of these events had to be controlled in the lab to successfully fertilize eggs from cows.

Proteins produced in the seminal vesicles, prostate, and Cowper’s glands convey the capacitating effects of heparin, a carbohydrate, to bull sperm. Those proteins are collectively referred to a heparin-binding proteins because they function as “docking’ molecules to allow heparin to physically attach to the sperm, causing capacitation. Heparin per se is not found in the female reproductive tract. However, several other heparin-like carbohydrates do exist, and heparin mimics their normal biological action.

One specific heparin binding protein has been named fertility-associated antigen (FAA). For the past 13 years, research has focused specifically on FAA, its identity, the ability to detect it in semen, and field trials comparing fertility of bulls classified as FAA-positive or FAA-negative. Trials included multiple-sire pastures with or without parentage of calves being confirmed by DNA testing. Herds have utilized A.I. in some instances, and serving capacity was also evaluated one year before bulls were allocated to pastures.

Field Trials Comparing Bulls Categorized as FAA-Positive or FAA-Negative

Since 1992, field trials have been conducted in Texas, Nebraska and California to compare prolificacy of bulls that produced semen classified as FAA-positive or FAA-negative. Multiple-sire pastures: Table 1 contains data from 7 consecutive years of field trials at King Ranch. When bulls were 14-19 mo. of age, FAA status was determined after they passed a breeding soundness exam. All pastures contained 8-16 bulls for 60d at a constant ratio of 1 bull per 25 cows. Overall, FAA-positive bulls were 19 percentage points more fertile than their FAA-negative herdmates. FAA was quantified in the Ax lab at the University of Arizona.

Serving capacity and FAA: The ability of a bull to breed cows can be estimated as “serving capacity.” This is ordinarily evaluated by placing a group of virgin bulls with heifers that were synchronized to be in heat. Mounts with penetration are scored for each bull over a period of 20 min. Bulls are then ranked as “high” or “low” in that social setting.

FAA-positive bulls with high serving capacity impregnated 87% of cows exposed to them for a 60d breeding season. FAA positive bulls with low serving capacity only impregnated 69% of the exposed cows. Bulls with semen lacking FAA but with high serving capacity impregnated 78% of the cows pastured with them. Therefore, their libido was able to compensate for the absence of FAA, but they were inferior to herdmates with high serving capacity possessing seminal FAA (Table 2). FAA was measured in the University of Arizona Lab. A.I. outcomes: With A.I., serving capacity is not an issue because cows are inseminated when they are in estrus. Holstein heifers and range beef cows were inseminated once with semen from mixed breeds of beef bulls designated as FAA-positive (n=18) or FAA-negative (n=7). Overall, there was a 16% higher fertility in females inseminated with FAA-positive semen (66% pregnancy rate) compared to FAA-negative semen (50% pregnancy rate, Table 3). The University of Arizona Lab analyzed semen for FAA content.

Efficiency of the cow herd: What does selection for FAA-positive bulls do for the cow herd? Research obtained from 1992 through 1998 at King Ranch indicated that the distribution of calves born during the calving season shifted to births occurring earlier (Table 4). In the nucleus herd, cows were initially bred only to FAA-positive bulls. Their replacement daughters were also only bred to FAA-positive bulls in subsequent generations. By 1998, 22% more calves were born in the first 20 days of the calving season from this FAA selection management practice (Table 4). Clearly, efficiency in the cow herd had improved.

DNA parentage of calves: In a collaboration with Drs. Dave and Cindy Daley and Harris Ranches, FAA status of bulls was determined using a newly developed chute-side cassette. Those bulls were in multiple-sire pastures with cows for a 60-day breeding season in 3 consecutive breeding years (2000, 2001, 2002). The trial was conducted to relate parentage of calves by DNA fingerprinting to growth and carcass traits of individual sires. Analysis of FAA status became a retrospective comparison to evaluate utility of the cassettes to analyze semen for FAA within 20 minutes.

Results from this study are being analyzed. Overall, 12 out of 62 total bulls were found to be FAA-negative. This was close to the incidence found in a population of 914 bulls screened in 6 states in April, 2003. In those bulls, 26% were FAA-negative using the same test cassette to quantify FAA in semen.

With the Harris Ranch bulls, complete DNA profiles were achieved with 47 of the 62 bulls. Overall, as bulls got older, they sired more calves per bull (1.1 as yearlings to 22.2 as 5-year old breeding bulls). Irrespective of age, FAA-positive bulls produced 5.9 more calves in the 3 years (1.9 calves/year) compared to FAA-negative herdmates. That translated into a 19% higher calf production for FAA-positive bulls for the 3-year duration of the trial (Table 5). There was clearly an age influence in terms of calf production in relation to FAA status of bulls. As yearlings and 5-year olds, FAA status did not factor into calf yield. However, between the ages of 2 and 4, each FAA-positive bull averaged 35.4 total calves, whereas his FAA-negative herdmates produced 27.3 total calves in that period of time. Therefore, the FAA-negative bulls were 77% as prolific as their FAA-positive contemporaries based upon those numbers.

From ages 1 through 3 years, a higher proportion of FAA-negative bulls were more likely to not sire any calves compared to FAA-positive bulls. In other words, sterility of a bull in a given year corresponded to FAA status of bulls 3 years old or younger.

CONCLUSION

FAA is a good thing! Fertility data support that regardless of years, pasture, or breed, the FAA positive bulls resulted in a higher percentage of cows pregnant compared to FAA negative herdmates. A conservative estimate places pregnancy rates 15% higher in heifers or cows bred to FAA positive bulls.

The calving season should also tighten up if daughters are retained from FAA positive bulls and are bred to known FAA positive bulls. In tern, daughters in subsequent generations need to be bred to FAA positive bulls, and that practice should continue.

FAA testing only takes 20 minutes and is based upon visible detection of a reddish-purple line on a plastic cassette that contains all the necessary chemicals to detect FAA if it is in a semen sample. The projected payback per cow in a herd from testing for FAA in bulls will be 16 to -25 fold if net profit per calf is $50.00. Obviously, if profit per cow exceeds $50.00, then the value of testing for FAA increases substantially.

For more information, pricing, and to order testing kits, contact:

ReproTec, Inc. (520) 888-0401 (520)888-0297 (FAX) www.reprotec.us

Suggested Readings

1. Ax, R.L., H.E. Hawkins, S.K. DeNise, T.R. Holm, H.M. Zhang, J.N. Oyarzo and M.E. Bellin. 2002. New Developments in Managing the Bull. In: Factors Affecting Calf Crop. M.J. Fields, R.S. Sand, J.V. Yelich (eds.), CRC Press, Boca Raton, Chap. 21, pp. 287-296.

2. Bellin, M.E., H.E. Hawkins and R.L. Ax. 1994. Fertility of Range Beef Bulls Grouped According to Presence or Absence of Heparin-Binding Proteins in Sperm Membranes and Seminal Fluid. J Anim Sci 72: 2441-2448.

3. Bellin, M.E., H.E. Hawkins, J.N. Oyarzo, R.J. Vanderboom and R.L. Ax. 1996. Monoclonal Antibody Detection of Heparin-Binding Proteins on Sperm Corresponds to Increased Fertility of Bulls. J Anim Sci 74: 173-182.

4. Bellin, M.E., J.N. Oyarzo, H.E. Hawkins, H. Zhang, R.G. Smith, D.W. Forrest, L.R. Sprott and R.L. Ax. 1998. Fertility-Associated Antigen on Bull Sperm Indicates Fertility Potential. J Anim Sci 76: 2032-2039.

5. McCauley, T.C., H.M. Zhang, M.E. Bellin and R.L. Ax. 1999. Purification and Characterization of Fertility-Associated Antigen (FAA) in Bovine Seminal Fluid. Mol Reprod Dev 54: 145-153.

6. McCauley, T.C., G.R. Dawson, J.N. Oyarzo, J. McVicker, S.H.F. Marks and R.L. Ax. 2004. Development and Validation of a Lateral-flow Cassette for Fertility Diagnostics in Bulls. In Vitro Diagnostic Technology, In Press.

7. Miller, D.J. and R.L. Ax. 1990. Carbohydrates and Fertilization in Animals. Mol Reprod Dev 26:184-198.

8. Sprott, L.R., M.D. Harris, D.W. Forrest, et al. 2000. Artificial Insemination Outcomes in Beef Females Using Bovine Sperm with a Detectable Fertility-Associated Antigen. J Anim Sci 78: 795-798.

Cryptosporidium parvum (C. parvum) is a protozoal parasite that can cause gastrointestinal illness in a wide variety of mammals, including humans, livestock, companion animals, and wildlife. New species of Cryptosporidium are constantly being discovered, such as C. canis and C. felis, but their significance relative to the large role that C. parvum plays in livestock and human cryptosporidiosis is still unclear. In the majority of livestock species, clinical disease and shedding of C. parvum typically occurs in youngstock under a few months of age, but fecal shedding of oocysts can also occur in healthy older animals which can then serve as a source of infection for these younger animals. In humans, clinical disease and shedding can appear at all ages, but is typically more common among children. The predominant clinical sign is profuse, watery diarrhea lasting from a few days to several weeks in normal (immunocompetent) individuals, but can be prolonged and life threatening among immunocompromised hosts such as AIDS patients. Modes of transmission range from direct fecal-oral transmission, as might occur between infected and susceptible calves during lay behavior, or ingestion of food or water inadvertently contaminated with oocysts from the feces of an infected host.

Waterborne transmission of the pathogenic protozoa, Cryptosporidium parvum, has emerged as an important public health concern. Because the infectious stage of C. parvum (oocysts) is resistant to conventional water treatment processes, public health agencies and water districts are actively seeking methods of reducing surface water contamination with this parasite. Protection of source water such as rivers and lakes has the potential to reduce the risk of transmission to humans and animals through drinking water, as well as through human recreational contact with untreated water. Given that the parasite readily infects a large number of mammalian hosts (Fayer et al. 1997), there are a number of possible contributing sources of oocysts present for any given watershed. Unfortunately, the primary quantitative sources of waterborne C. parvum oocysts are not well defined, and our methods of prioritizing point and non-point vertebrate sources of this zoonotic parasite are lacking.

Our objective is to develop a standardized methodology for comparing environmental loading rates for different populations of vertebrate hosts for C. parvum. Such a comparison would help form the basis of a rational decision making process for evaluating land use practices and vertebrate populations with respect to their relative environmental loading rates for important waterborne microbial pathogens. Both domestic and wild animal populations are infected by and can shed in their feces the infectious stage of this parasite. Attempting to characterize or assess the risk of point and non-point source protozoal contamination requires numerous parameters to be estimated, the most important being a valid and precise estimate of the oocyst loading rate per animal unit (Atwill et al. 2001; Hoar et al. 2000). The oocyst loading rate, which can be defined as the total number of oocysts excreted by a defined cohort of animals for a specific period of time, can be calculated directly by measuring the kinetics of total oocyst shedding, that is, duration and intensity per Kg feces, multiplied by fecal production. This direct measurement method is very difficult for free-ranging wildlife and some species of livestock. An alternative approximation for determining the oocyst loading rate for cohorts of mammals is to measure the prevalence of infection and the intensity of shedding using cross-sectional surveys of the mammalian population, and then relying on experimental or laboratory estimates of fecal production (Hoar et al. 2000). We applied these concepts to a variety of domestic and wild animal species to generate a set of comparative loading rates for the waterborne pathogen, C. parvum.

A great deal has been learned about foraging behavior and livestock distribution in the last several decades. We hope to apply and fine tune this knowledge to reduce the impacts of beef cattle on riparian areas, surface water and wildlife habitat. Likewise, to use cattle as a tool to manage weeds we need to be able to attract cattle into patches of undesirable species.

Beef cattle and other grazers focus on water sites and sites that provide thermal comfort, foraging away from these focal points to meet their nutritional needs. Most ungulates first harvest food, then move either to loafing and bedding sites to ruminate and digest the food ingested in a previous grazing bout (meal), and/or to areas for predator avoidance. The distance covered by the animal during foraging depends on digestive capacity, rate of passage, forage harvest rate, grazing velocity and level of hunger. Once satisfied the animal returns to a thermal, water or bedding site depending on their needs and priorities.

Time spent grazing depends on forage availability, forage quality, and thermal balance. Animals reduce daily grazing time as digestibility of available forage declines and retention time of ingesta increases. When daytime temperatures are within the thermal comfort zone of cattle, most grazing takes place during daylight hours. During hot weather cattle reduce afternoon grazing and increase night-time grazing. Most researchers report little grazing and traveling after darkness. However, recent nighttime observations at San Joaquin Experimental Range in Madera County indicate that grazing and change of bedding sites do occur during darkness on some nights. The objective of this study at UC SFREC is to understand where beef cattle distribute themselves in a typical foothill oak woodland or annual grassland during a 24 hour period and how this may change seasonally. Studies on private ranches are underway to document the effectiveness of protein supplement sites as attractants for beef cattle at different distances from stock water and riparian areas.

All publications resulting from research conducted at Sierra Foothill Research & Extension Center from 1969 to 2003.