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Heat Stress Management with OmniGen Nutritional Specialty Product

Heat Stress Management with OmniGenTM Nutritional Specialty Product

Cattle are susceptible to a wide range of stressors on the farm, heat being one of the most common. Being proactive is the best approach to help manage the short- and long-term consequences of heat stress. OmniGen nutritional specialty product from Phibro Animal Health can help protect your herd from the negative impacts of stress caused by typical heat stress conditions. Click on this video to learn more.

Nutritional and Management Considerations Before, During & After Heat Stress

Keep Cool

Dairy Cow Immunity Impacts Reproductive Performance – Advisory

DAIRY COW IMMUNITY IMPACTS REPRODUCTIVE PERFORMANCE

A. Rowson, DVM and D. Kirk, Ph.D., PAS
Phibro Animal Health Corporation, Quincy, IL

Impaired reproductive performance of dairy cows can have significant impact on the profitability of dairy operations.  The immune system has been shown to play a role in dairy cow reproduction, both indirectly, through the effects of mastitis, metritis, retained placenta, and metabolic diseases; and directly, through actions of immune cells upon the ovary.  A properly-functioning immune system may help improve reproductive performance of dairy cattle by reducing occurrence of diseases affecting fertility, and improving immune cell activity.

REVIEW OF DAIRY COW REPRODUCTION

The cow’s estrous cycle is approximately 21 days long.  It is divided into two phases which are characterized by changes on the ovary.  The follicular phase makes up 20% of the cycle.  During this phase the pre-ovulatory follicle on the ovary, which contains the oocyte (or egg), produces estrogen.  When estrogen concentrations are high enough, a surge of luteinizing hormone (LH) is released, initiating ovulation. The luteal phase begins after ovulation, when the follicle transforms into a corpus luteum (CL) which produces progesterone to maintain pregnancy.  This phase makes up the remaining 80% of the estrous cycle.

 

Reproductive performance is monitored using several metrics:
Calving Interval   Period between calvings
Days Open   Period between calving and confirmed conception
Services Per Conception   Total services per total number of pregnant cows
Heat Detection Rate   Percent of eligible cows that are bred
Conception Rate   Percent of cows bred that are pregnant
Pregnancy Rate   Percent of cows eligible to become pregnant that are confirmed pregnant during a given period (usually 21 days)

 

Reproductive performance is affected by both breeding success and pregnancy loss. Typically, gestation lasts 280 days. Up to 40% of pregnancies are lost in first 17 days of gestation. Early embryonic loss occurs from 0 to 15 days of gestation, and is usually not detected since pregnancy loss at this stage does not delay estrus. Late embryonic loss occurs at 16 to 41 days of gestation, and will delay ovulation and thus extend the estrous cycle. Embryonic losses usually occur before pregnancy is confirmed. Abortion occurs between 42 to 260 days of gestation, and stillbirths occur from 260 days of gestation through birth. “Normal” abortion rates are 3% to 5% per year.

INDIRECT EFFECTS OF DISEASE ON REPRODUCTION IN DAIRY COWS

Mastitis is associated with: increased Days Open1,2; greater Services/Conception2; reduced Conception Rate3,1; reduced Pregnancy Rate4,1; higher incidence of Early Embryonic Death5,6; and greater risk of abortion7,1. Infection of the udder affects the structure and function of the ovaries8 and has also been associated with altered patterns of reproductive hormone secretion4. These effects may be linked to a systemic response by cytokines9 (molecules released by cells that affect actions of other cells, particularly immune cells) which may also lead to pregnancy loss10.

Retained placenta can also have indirect effects upon fertility, including: reduced Conception Rate3; lower Pregnancy Rate11; more Services per Conception12; and increased Days Open13. Retained placenta is associated with reduced neutrophil function and lower blood concentrations of interleukin-814 (IL-8, a cytokine that attracts immune cells to sites of infection), and may alter activities of the CL15.

Uterine disease, which includes metritis (inflammation of the entire uterus) and endometritis (inflammation of the uterine lining), is associated with: lower Conception Rate16; reduced Pregnancy Rate11; and increased Days Open17. Uterine disease appears to have the greatest impact on fertility by reducing ovulation rate18 and CL size19 during the first post-partum estrous cycle. Cows with uterine disease also have smaller follicles and lower blood estrogen concentrations20. Cows that develop uterine disease experience reduced neutrophil function around the time of calving21,22.

Metabolic diseases are also associated with impaired reproductive performance.

  • Milk fever increases Days to 1st Service11
  • Subclinical hypocalcemia reduces 1st Service Conception Rate23
  • Ketosis increases Days to 1st Service & decreases 1st Service Conception Rate11
  • Mastitis combined with other diseases has greater negative impact on reproduction than any one disease alone24

IMMUNE CELLS PLAY A DIRECT ROLE IN REPRODUCTION
Immune cells, primarily neutrophils, macrophages, and T-lymphocytes, are required by the ovary for normal ovulation and CL function25. Activities of these immune cells are regulated by the luteal environment, and result in both CL development and regression26. Neutrophils migrate into the early CL (day 1 to 4 of the estrous cycle), in response to IL-8 produced by the CL. Neutrophil numbers and IL-8 concentrations are low at the mid- and late-luteal phase but IL-8 is high at luteal regression. Interestingly, cortisol (a potent, immunosuppressive hormone released in response to stress) acts to block the release and peak of LH from the pituitary gland, which can prevent ovulation.

The immune system has both direct and indirect effects upon reproduction in dairy cows. Reproductive performance may be improved with a properly-functioning immune system.

REFERENCES
1Santos, J. E. P., R. L. A. Cerri, M. A. Ballou, G. E. Higginbotham, J. H. Kirk. 2004. Effect of timing of first clinical mastitis occurrence on lactational and reproductive performance of Holstein dairy cows. Animal Reproduction Science 80:31–45.

2Schrick, F. N., M. E. Hockett, A. M. Saxton, M. J. Lewis, H. H. Dowlen, and S. P. Oliver. 2001. Influence of subclinical mastitis during early lactation on reproductive parameters. J. Dairy Sci. 84:1407–1412.

3Hertl, J. A., Y. T. Gröhn, J. D. G. Leach, D. Bar, G. J. Bennett, R. N. González, B. J. Rauch,
F. L. Welcome, L. W. Tauer, and Y. H. Schukken. 2010. Effects of clinical mastitis caused by gram-positive and gram-negative bacteria and other organisms on the probability of conception in New York State Holstein dairy cows. J. Dairy Sci. 93:1551–1560.

4Hockett, M. E., R. A. Almeida, N. R. Rohrbach, S. P. Oliver, H. H. Dowlen, and F. N. Schrick. 2005. Effects of Induced Clinical Mastitis During Preovulation on Endocrine and Follicular Function. J. Dairy Sci. 88:2422–2431.

5Chebel, R. C., J. E. P. Santos, J. P. Reynolds, R. L. A. Cerri, S. O. Juchem, and M. Overton. 2004. Factors affecting con- ception rate after artificial insemination and pregnancy loss in lactating dairy cows. Anim. Reprod. Sci. 84:239.

6Moore, D. A., M. W. Overton, R. C. Chebel, M. L. Truscott, and R. H. BonDurant. 2005. Evaluation of factors that affect embryonic loss in dairy cattle. J. Am. Vet. Med. Assoc. 226:1112.

7Risco, C. A., G. A. Donovan, and J. Hernandez. 1999. Clinical mastitis associated with abortion in dairy cows. J Dairy Sci. 82:1684–1689.

8Rahman, M. M., M. Mazzilli, G. Pennarossa, T. A. L. Brevini, A. Zecconi, and F. Gandolfi. 2012. Chronic mastitis is associated with altered ovarian follicle development in dairy cattle. J. Dairy Sci. 95:1885–1893.

9Chebel, R. C. 2007. Mastitis effects on reproduction. NMC Regional Meeting Proc. (2007):43–55.

10Soto, P., R.P. Natzke, and P.J. Hansen. 2003. Identification of possible mediators of embryonic mortality cause by mastitis: actions of lipopolysaccharide, prostaglandin F2α, and the nitric oxide generator, sodium
nitroprusside dihydrate, on oocyte maturation and embryonic development in cattle. Am. J. Reprod. Immunol. 50:263.

11Fourichon, C., H Seegers, and X. Malher. 2000. Effect of disease on reproduction in the dairy cow: a meta-analysis. Theriogenology 53:1729–1759.

12Joosten, I., J. Stelwagen, A. A. Dijkhuizen. 1988. Economic and reproductive consequences of retained placenta in dairy cattle. Veterinary Record 123, 53–57.

13Yeon-Kyung, H and K. Ill-Hwa. 2005. Risk factors for retained placenta and the effect of retained placenta on the occurrence of postpartum diseases and subsequent reproductive performance in dairy cows. J. Vet. Sci. 6(1), 53–59.

14Kimura, K., J. P. Goff, M. E. Kehrli, Jr. and T. A. Reinhardt. 2002. Decreased Neutrophil Function as a Cause of Retained Placenta in Dairy Cattle. J. Dairy Sci. 85:544–550.

15Holt, L. C., W. D. Whittier, F. C. Gwazdaukas, and W. E. Vinson. 1989. Early Postpartum Reproductive Profiles in Holstein Cows with Retained Placenta and Uterine Discharges. J. Dairy Sci. 72:533–539.

16Dubuc, J., T. F. Duffield, K. E. Leslie, J. S. Walton, and S. J. LeBlanc. 2011. Effects of postpartum uterine diseases on milk production and culling in dairy cows. J. Dairy Sci. 94:1339–1346.

17Giuliodori, M. J., R. P. Magnasco, D. Becu-Villalobos, I. M. Lacau-Mengido, C. A. Risco, and R. L. de la Sota. 2013. Metritis in dairy cows: Risk factors and reproductive performance. J. Dairy Sci. 96:3621–3631.

18Herath, S., H. Dobson, C. E. Bryant, and I. M. Sheldon. 2006. Use of the cow as a large animal model of uterine infection and immunity. Journal of Reproductive Immunology 69 (2006) 13–22.

19Strüve, K., K. Herzog, F. Magata, M. Piechotta, K. Shirasuna, A. Miyamoto and H. Bollwein. 2013. The effect of metritis on luteal function in dairy cows. BMC Veterinary Research 9:244–252.

20Sheldon, I. M., E. J. Williams, A. N. A. Miller, D. M. Nash, S. Herath. 2008. Uterine diseases in cattle after parturition. The Veterinary Journal 176:115–121.

21Cai, T. Q., P. G. Weston, L. A. Lund, B. Brodie, D. J. McKenna, and W. C. Wagner. 1994. Association between neutrophil functions and periparturient disorders in cows. Am. J. Vet. Res. 55:934–943.

22Hammon, D. S., I. M. Evjen, T. R. Dhiman, J. P. Goff, and J. L. Walters. 2006. Neutrophil function and energy status in Holstein cows with uterine health disorders. Vet. Immunol. Immunopath. 113:21–29.

23Chapinal, N., M. E. Carson, S. J. LeBlanc, K. E. Leslie, S. Godden, M. Capel, J. E. P. Santos, M. W. Overton, and T. F. Duffield. 2012. The association of serum metabolites in the transition period with milk production and early-lactation reproductive performance. J. Dairy Sci. 95:1301–1309.

24Ahmadzadeh, A., M. A. McGuire, J. C. Dalton. 2010. Interaction between Clinical Mastitis, Other Diseases and Reproductive Performance in Dairy Cows. WCDS Advances in Dairy Technology Volume 22:83–95.

25Walusimbi, S. S., and J. L. Pate. 2013. Physiology and Endocrinology Symposium: Role of immune cells in the corpus luteum. J. Animal Sci., 91:1650-1659.

26Jiemtaweeboon, S., K. Shirasuna, A. Nitta, A. Kobayashi, H. J. Schuberth, T. Shimizu and A. Miyamoto. 2011. Evidence that polymorphonuclear neutrophils infiltrate into the developing corpus luteum and promote angiogenesis with interleukin-8 in the cow. Reproductive Biology and Endocrinology 9:79–88.

 

OG010215 © 2015 Phibro Animal Health Corporation.

Beat the heat this summer

Beat the heat this summer

It has long been known that heat stress adversely affects production and reproduction in dairy cows worldwide. In the United States alone, Normand St-Pierre and co-workers at The Ohio State University have estimated that annual economic losses to heat stress in the dairy industry exceed $900 million per year.

A 2002 report estimated that 48 percent of dairy cows, or 4.2 million, in the United States are subjected to thermal or heat stress on an annual basis, negatively affecting milk yield, reproduction and health. Heat stress is unique in that it not only raises net energy requirements for maintenance but simultaneously reduces intake, which exacerbates the milk yield decline attributed to it.

However, not all of the reduction in milk yield during heat stress is associated with reduced feed intake. Research by Baumgard and Rhoads at the University of Arizona demonstrated that more than half of the milk loss in heat-stressed dairy cows is unrelated to a reduction in dry matter intake. Furthermore, the dairy cow shifts its metabolic fuel consumption during heat stress, burning more glucose and fewer nonesterified fatty acids.

The cow’s “lack of ability” to utilize body fat as a fuel during heat stress seems to be a metabolic adaptation to, in essence, preserve itself. Considerable work remains to further define the most effective nutritional strategies to minimize the impacts of heat stress on production in lactating dairy cows and to fully understand the metabolic alterations that occur in heat-stressed dairy cows.

Help them lose heat

Basic strategies to reduce the impact of heat stress include altering the environment around the cow by reducing heat gain (providing shade) and elevating heat loss (fans, soakers and evaporative cooling). In addition, producers and their advisers employ a number of nutritional strategies to maximize energy intake during periods of thermal stress. These include altering feeding times to allow more feed intake at night when it is cooler, increasing the energy density of the ration to reduce gut fill, providing high-quality forages and using total mixed rations to reduce feed sorting by cattle.

In addition to production losses, disease incidence and the immune system are compromised in heatstressed cows. This is associated with the release and elevation of cortisol common at the initial exposure to heat. Dry matter intake is compromised, and the cow’s mechanisms to digest and utilize nutrients are altered. As the cow’s system works to get rid of heat, it shunts nutrients to its extremities to aid in heat dissipation.

In reducing the cow’s heat load, nutrients are “freed up” to be utilized for more productive tasks, such as milk production, reproduction and immune function. Utilizing strategies to help cows deal with heat dissipation physically, with well-defined management protocols and, metabolically, with proven nutrition programs, alleviates the severity of heat stress and supports a faster recovery of the immune system. With this reduction in heat stress that the cow perceives, cortisol levels will begin to return to normal. This may result in improved health and productivity after periods of heat stress.

As dairy producers make plans to prepare for heat stress season, it’s important to double check the operation of and clean all fans, and test and service sprinklers, soakers or evaporative cooling systems. Work with your nutritionists to plan for necessary ration changes. When considering new or novel nutritional strategies to support normal health and immune status during heat stress, ask for a review of supporting research before making a final decision.

Authors

J.P. Jarrett

R.J. Collier

Stress & Health (Part 1 of 2)

Relationship Between Stress and Health in Cattle

Part 1

Jeffery A. Carroll, PhD and Nicole C. Burdick Sanchez, PhD
Livestock Issues Research Unit, USDA-ARS

Introduction

Today, the scientific community and producers alike acknowledge the fact that “stress” can potentially have detrimental effects on animal productivity, and overall health and well-being (Carroll and Forsberg, 2007).
Even though the debate among animal scientists concerning the definition and quantification of “stress” is ongoing, an increased understanding and appreciation with regard to the effects of
“stress” on livestock production now exists both within the scientific community and with livestock producers.
While the physiological consequences of “stress” on the body have been of scientific interest for many years, scientists have yet to fully elucidate the complex interactions among stress hormones and the immune system. However, there is substantial literature available documenting the detrimental effects of prolonged stress on the immune system and overall health of livestock (Moberg, 1987; Dobson et al., 2001; Shi et al., 2003).

So What is “Stress”?

Stress, as it relates to bodily functions, has been defined as the sum of all biologic reactions to physical, emotional, or mental stimuli that disturb an individual’s homeostasis. Therefore, a stressor can be defined as any internal or external stimuli or threat that disrupts homeostasis of the body, and elicits a coordinated physiological response in an attempt to reestablish
homeostasis.

Maintaining a state of homeostasis requires proper functioning of all physiological processes including the stress and immune systems which are influenced by numerous factors including
environmental conditions, pathogen exposure, genetic makeup, animal temperament, and nutrient availability.

Research related to “stress” in domestic animals continues to evolve and expand, with emergent multidisciplinary efforts leading to a greater understanding of homeostatic regulation. Not only has the definition of “stress” been refined and updated based upon continued scientific discoveries, but the perception of “stress” in domestic animals has evolved as well.

Stress, as we now know, includes indices such as environmental stress, nutritional stress, social stress, and even prenatal stress. Animal stress is now identified as a unique event that elicits a
specific behavioral, physiological, neuroendocrine, endocrine, and/or immune response that may be as unique as the stressful event itself.

There has been an increased effort to elucidate the interactions between stress responsiveness and immunological parameters in cattle that may be either predisposed to or resistant to the
detrimental effects of stress due to genetic programming and/or prior experiences.

Interestingly, there are cattle that demonstrate differential stress and immunological responses due to previous exposure to various managerial, environmental, nutritional, or pathogenic stressors or due to varying temperaments within a genetically similar group of animals (Carroll and Forsberg, 2007; Burdick et al., 2011; Burdick et al., 2012).

Cortisol and Animal Health

Often considered the second line of defense is the suppression of the primary immune defense by cortisol.

Suppression of the inflammatory and immune systems by cortisol prevents excessive and chronic stimulation of these systems which could prove deadly to the animal. Specifically, cortisol suppresses the release of various cytokines produced by cells of the immune system which can cause systemic disease.

Chronic exposure to high concentrations of cortisol can cause severe physiological and psychological problems such as excessive protein catabolism, hyperglycemia, immunosuppression, and depression.

In domestic livestock, excessive concentrations of cortisol have been linked to reduced rates of reproduction, suboptimal growth, suppressed milk production, and suppression of immune function that could increase susceptibility to disease (Lay et al., 1992; Buckham Sporer et al., 2008).

Depending upon the production system, cattle may be exposed to numerous stressors for varying durations that can significantly inhibit both health and productivity.

As researchers have continued to explore the complex interactions between stress and production parameters such as growth, reproduction, and health, multidisciplinary efforts have emerged that have led to a greater understanding of homeostatic regulation. Based upon these efforts, our knowledge has extended beyond the “all or none” biological activity strictly associated with the “fight or flight” response.

For instance, researchers have demonstrated that the combined immunological effects of cortisol and catecholamines result in a wellorchestrated biological event designed to prevent over-stimulation of innate immunity and the production of proinflammatory cytokines while simultaneously priming the humoral immune response in an effort to provide adequate immunological protection.

Conclusion

The detrimental effects caused by stressors encountered by livestock during routine handling can pose economic problems for the livestock industry due to increased costs ultimately borne by both the producer and the consumer.

Increased secretion of stress-related hormones in response to handling during management procedures may be harmful, as these hormones may inhibit physiological systems such as immunity.

Therefore, an understanding of the interaction between the stress and immune systems, and their subsequent impact on growth, is necessary in order to reduce negative impacts on growth and productivity in livestock.

References

Buckham Sporer, K.R., P.S.D. Weber, J.L. Burton, B. Early, and M.A. Crowe. 2008. Transportation of young beef bulls alters circulating physiological parameters that may be effective biomarkers of stress. J. Anim. Sci. 86:1325-1334.

Burdick, N.C., R.D. Randel, J.A. Carroll, and T.H. Welsh, Jr. 2011. Interactions between temperament, stress, and immune function in cattle. Int. J. Zool. 1-9.

Burdick, N.C., R. Chaffin, J.A. Carroll, C.C. Chase, Jr., S.W. Coleman, and D.E. Spiers. 2012. Influence of heat stress on the immune response of Angus and Romosinuano heifers to an LPS challenge. J. Anim. Sci. 90(E-Suppl.2):22 (Abstract # 67).

Carroll, J.A., and N.E. Forsberg. 2007. Influence of stress and nutrition on cattle immunity. Vet. Clin. North Am. Food. Anim. Pract. 23:105-149.

Dobson, H., J.E. Tebble, R.F. Smith, W.R. Ward. 2001. Is stress really all that important? Theriogenology. 55:65-73.

Lay Jr., D.C., T.H. Friend, R.D. Randel, C.L. Bowers, K.K. Grissom, and O.C. Jenkins. 1992. Behavioral and physiological effects of freeze or hot-iron branding on crossbred cattle. J. Anim. Sci. 70:330-336.

Moberg, G.P. 1987. A model for assessing the impact of behavioral stress on domestic animals. J. Anim. Sci. 65:1228-1235.

Shi, Y., S. Devadas, K.M. Greeneltch, D. Yin, R.A. Mufson, and J. Zhou. 2003. Stressed to death: implication of lymphocyte apoptosis for psychoneuroimmunology. Brain, Behav. Immun. 17, S18-S26.

StressPart1-Figure1

Figure 1: When an animal perceives either an internal or external threat, neurotransmitters are released in the brain that cause the release of corticotrophin-releasing hormone (CRH) and vasopressin (VP) that stimulate the release of adrenocorticotrophin (ACTH). ACTH in turn stimulates the release of cortisol, epinephrine (Epi) and norepinephrine (NE), each of which affect various target tissues in the body including the immune system (Carroll, J.A. and N.C. Burdick. 2011. Relationships between Stress and Health in Cattle. Phibro Animal Health Corporation. Advisory Bulletin, June 2011).

Stress & Health (Part 2 of 2)

Relationship Between Stress and Health in Cattle

Part 2

Jeffery A. Carroll, PhD and Nicole C. Burdick Sanchez, PhD
Livestock Issues Research Unit, USDA-ARS

Introduction

Numerous physiological and psychological conditions significantly influence the health and subsequent growth of livestock.

In domestic livestock, increased stress hormones in response to managerial stressors have been linked to reduced rates of reproduction, suboptimal growth, suppressed milk production, and
suppression of immune function that could increase susceptibility to disease (Lay et al., 1992; Buckham Sporer et al., 2008).

Through an understanding of the interactions between the stress system and immune function, animal management practices can be modified to reduce negative impacts on growth and productivity in livestock.

The Immune System

To aid in understanding the relationship between “stress” and animal health, it’s important to understand that the immune system is not a single entity, but rather a complex, integrated system regulated by a multitude of specialized cells and chemical messengers.

In general, however, the immune system can be separated into three broad components; natural immunity, innate immunity, and acquired immunity, all of which must be fully developed and functioning properly to provide adequate immunological protection.

Natural and innate immunity are typically grouped together under the category of innate immunity. Therefore, when discussing innate immunity, it is typically assumed that one is including natural immunity as well.

Innate immunity is considered to be the first line of defense against pathogens; whether bacterial, viral, protozoal or fungal. It includes physical barriers such as the skin, mucosal secretions, tears, urine, and stomach acid, as well as complement and antigen-nonspecific cellular components and is designed to elicit an immediate or acute response (0-to-4 hour) following exposure to an antigenic agent.

Until recently, the innate immune system was thought to represent the antigen-nonspecific aspect of the immune system. However, recent evidence suggests that the innate response may be specific to the pathogenic agent encountered.

While it is often assumed that this aspect of the immune system becomes a constant entity once developed by the animal, this is certainly not the case. The innate immune system, while always
present to some degree, can be modulated in either a beneficial or detrimental manner by a number of factors including wounds, dehydration, nutritional status, genetics, stress, and various peptide hormones (Figure 1).

Stress and the Immune System

As the scope of scientific exploration has expanded beyond traditionally defined pathways of neuroendocrinology, endocrinology, and immunology, multidisciplinary efforts emerged leading to the identification of cross-communication pathways among the stress and immune systems, and to a better understanding of homeostatic regulation within the animal.

No longer is stress considered strictly immuno-suppressive. Indeed, stress may elicit “bi-directional” effects on immune function such that acute stress may be immuno-enhancing, while chronic stress may be immuno-suppressive.

Today, our knowledge base has expanded, and a greater appreciation and understanding has emerged regarding the plethora of immune system activities that are influenced by cortisol such as stimulation of immune system chemical messengers, and stimulation of immune
cell growth and function (Figure 2).

In addition to these stimulatory actions, long-term exposure to cortisol is known to inhibit aspects of immune function. Ultimately, within the animal, the immune system response to
stress is dependent upon the type of stress encountered (i.e., acute versus chronic).

In some instances of acute stress, such as that resulting from bites, punctures, scrapes or other challenges to the integrity of the body, stress hormones are associated with priming the immune system in a manner to prepare for potentially invading pathogens and subsequent infection.

However, when an animal experiences prolonged or “chronic” stress, the effect of stress hormones on the immune system shifts from a preparatory event to a series of suppressive events; first at the cellular level and then eventually across the entire immune system spectrum.

While the discussion pertaining to the influences of stress on the immune system have been primarily focused on the actions of cortisol, one cannot discount the involvement of the catecholamines, epinephrine and norepinephrine, as modulators of the immune system.

An increase in circulating concentrations of catecholamines following a stressful event has been previously reported to modulate immune cell activities such as proliferation, cytokine and antibody production, cytolytic activity, and cell migration.

Continued research efforts into these complex interactions may allow the implementation of alternative management practices, improved selection programs, and/or implementation of various nutritional strategies to prevent or overcome significant production losses and animal health care costs for livestock producers.

References

Buckham Sporer, K.R., P.S.D. Weber, J.L. Burton, B. Early, and M.A. Crowe. 2008. Transportation of young beef bulls alters circulating physiological parameters that may be effective biomarkers of stress. J. Anim. Sci. 86:1325-1334.

Burdick, N.C., B.C. Bernhard, J.A. Carroll, R.J. Rathmann, and B.J. Johnson. 2012. Enhancement of the acute phase response to a lipopolysaccharide (LPS) challenge in steers supplemented with chromium. Innate Immunity. 18(4):592-601.

Bernhard, B.C., N.C. Burdick, W. Rounds, R.J. Rathmann, J.A. Carroll, D.N. Finck, M.A. Jennings, T.R. Young, and B.J. Johnson. 2012.

Chromium supplementation alters the performance and health of feedlot cattle during the receiving period and enhances their metabolic response to a lipopolysaccharide (LPS) challenge. J. Anim. Sci. doi:10.2527/jas.2011-4981).

Carroll, J.A., and N.E. Forsberg. 2007. Influence of stress and nutrition on cattle immunity. Vet. Clin. North Am. Food. Anim. Pract. 23:105-149.

Lay Jr., D.C., T.H. Friend, R.D. Randel, C.L. Bowers, K.K. Grissom, and O.C. Jenkins. 1992. Behavioral and physiological effects of freeze or hot-iron branding on crossbred cattle. J. Anim. Sci. 70:330-336.

variations

Figure 1: Factors that can have a significant influence on the function of the innate immune system of cattle. Naturally occurring deviations in the innate immune system, as well as the influence of various management practices on the immune system, are often overlooked in production systems (Carroll, J.A. and N.C. Burdick. 2011. Relationships between Stress and Health in Cattle. Phibro Animal Health Corporation Advisory Bulletin, June 2011).

LPS

Figure 2. The body’s response to an antigen includes increases in stress hormones and body temperature. Cortisol and catecholamines, as well as cytokines released from immune cells, stimulate an increase in body temperature in an effort to kill invading pathogens. The above figure depicts increases in rectal temperature and serum cortisol in cattle following exposure to lipopolysaccharide (LPS). (Burdick et al., 2011.)

Steer Body Green

Figure 3. In response to an immune challenge, body resources are redirected away from growth towards the immune system, resulting in a decrease in body weight. When challenged with lipopolysaccharide (LPS), a component of the cell wall of gram-negative bacteria (e.g., Escherichia coli), steers exhibited a 4.2% decrease in body weight within 24 hours (1 D Post). (Bernhard et al., 2012)

The Immune System of Ruminants

The Immune System of Ruminants

James D. Chapman, Ph.D. and Deb L. O’Connor, M.S., Dairy Technology Managers, Phibro Animal Health Corporation

Stress and Immunity in Dairy Cows

Immunity is defined by Dorland’s Illustrated Medical Dictionary, as security against a particular disease or nonsusceptiblilty to the invasive or pathogenic effects of foreign microorganisms or the toxic effect of antigenic substances. The immune system in the cow consists of two distinct but interactive systems; the innate and the adaptive or antibody mediated. Each of these has specific functions and response times but work in concert to protect the cow from infectious pathogens.

The innate system is composed of natural barriers (skin, stomach acids, enzymes, etc.) and white blood cells (neutrophils, macrophages) which continually monitor for sites of infection and pathogens and are the “first responders”. The adaptive or antibody system consists of other types of white blood cells whose function is to provide “long-term” protection against disease through the production of pathogen specific antibodies.

Stress has been defined as the sum of the biological reactions to any adverse stimulus; physical, mental, or emotional, internal or external, that tend to disturb or disrupt homeostatis, and should these compensating reactions be inadequate or inappropriate, they may lead to disorders or disease (Dorland’s Illustrated Medical Dictionary). Dairy cows can experience stress in a variety of ways, during dry off and calving, in extreme heat or cold conditions, sudden feed changes, etc. and the results of these ‘stressors’ may present itself as a case of mastitis, a retained placenta, an abrupt decline in milk production or an elevated somatic cell count.

Immune status or immune ‘health’ has been assessed using several immunological methods. One method is to assess total production of immunoglobulins (IgM and IgG’s). These are non-specific indicators of the combined titre against all antigens to which a cow is exposed. Another common measure is titre, which assesses T- and B-cell proliferation

and is an index of the adaptive immune systems ability to ‘ramp up’ to a specific chemical or mitogen challenge. More recently, scientists are using several more highly specific methods to assess immune system activity or ‘health’. These have focused on assays and procedures designed to assess the ability of certain white blood cells to kill pathogens via phagocytosis and the production of reactive oxygen species, or communicate with other immune cells through cytokine production, or maintain normal cell functions through the production of key proteins (L-selectin and interleukins) and cell surface receptors.

Research in the area of stress and immunity has shown that many components of the innate and adaptive immune systems are compromised during periods of stress. In particular, hormonal changes around the time of calving (figure 1.) can alter the ability of innate immune cells to respond and kill mastitis causing pathogens, through the inhibition of the production of L-selectin which is vital for normal neutrophil function (figure 2.). The detrimental effects of stress on immune function is not limited to those associated with parturition but can occur at any time and because of this it is important to initiate management and nutritional programs to reduce these events so cows are better to withstand pathogen challenges and maintain productivity.

Innate Immunity

The innate immune system represents the cow’s first line of defense against a pathogen challenge and provides the adaptive system the time required to develop the appropriate antibody response. Several components comprise the innate system, and they present barriers to pathogen entry and infection. These barriers consist of: 1) physical (skin, tears, gut and mammary cells); 2) chemical (stomach acid); 3) enzymatic (digestive); and 4) blood cellular components.

Neutrophils: “First Line of Defense”

Granulocytes and macrophages are predominantly white blood cells involved in innate immunity. Granulocytes are also called polymorphonuclear leukocytes (PMN), which are a diverse collection of white blood cells, including neutrophils. In the adult cow, there are approximately 200 billion neutrophils, half in circulation and the other half either attached to vessel walls or stored in bone. The life span of a neutrophil is short — 8 to 24 hours — and these white blood cells go through a process of self- destruction called apoptosis.

Figure 3. Toll-like receptors in cells. Eleven toll-like receptors have been identified and each
binds to a specific PAMP. Toll-like receptors 2 and 4 are responsible for identifying common molds as foreign.

The main function of neutrophils is to monitor for sites of infection and kill pathogens. Neutrophils identify pathogens by the recognition of distinct pathogen-associated molecular patterns (PAMPs). Specifically, pathogens contain molecules not typically found in mammalian cells and via this recognition of PAMPs neutrophils are able to find foreign cells. Examples of molecules associated with pathogens and recognized by neutrophils include lipotechoic acids, double-stranded RNA, CpG DNA sequences, and unusual sugar residues.

The neutrophil detects PAMPs by using specific receptors, called Toll-like receptors, which are located on their outer surface (Figure 3). Binding of PAMPs to Toll-like receptors initiates the killing mechanisms of neutrophils of which there are several. These include engulfing pathogens (phagocytosis), or entrapping them using projected strands of DNA called neutrophil extracellular traps or NETS and by respiratory bursts that involve the generation of several reactive oxygen species (ROS) which are bactericidal.

Adaptive or Antibody-Mediated Immunity

The primary function of the adaptive immune system is to develop antibodies against specific antigens. The time required for this response can be variable, ranging from a few days to several months, depending upon the antigen and the health of the cow. The antibodies produced in response to a foreign protein or antigen can be derived from a variety of cell types: T- and B-lymphocytes, antigen-presenting cells and Natural Killer (NK) cells.

Antibody Expressing Cells

B-cells mature in bone marrow (hence the name “B”) and are released into blood where they circulate and are captured by lymphoid tissue. These cells live less than 48 hours, unless they interact with their antigen (trigger activation), resulting in their proliferation and differentiation, a process termed “clonal selection.” The type of B-cell that can mature is driven by a process of “random gene rearrangement,” which can result in approximately 108 different types of B-cells, each with a specific target antigen.

Proliferation of a B-cell antigen-specific lineage is initiated following interaction with the antigen and requires input of interleukins-2, -4, -5, -6 and IFNy from T-helper cells. These cytokines cause formation of B memory cells from the activated B-cell population. Memory B cells can secrete as many as 2,000 antibody molecules/second into plasma. Antibodies may be of a variety of forms (e.g., IgG, IgM), which are targeted for specific purposes in the fight against pathogens. T-cells are manufactured in bone marrow and mature in the Thymus (hence the name “T”-cell). T-cells are responsible for “cell-mediated immunity” because the antibodies they manufacture remain attached (tethered) to the surfaces of the T-cell population. As in B-cells, interaction of a T-cell with a specific antigen causes clonal selection and expansion of a specific T-cell population that express as many as 100,000 antibody molecules on the surface of each cell. Clonal selection of T-cells, as with B-cells, leads to the development of “memory T-cells” (figure 5).

Antibodies

Antibodies consist of a Y-shaped molecule, containing a constant (C) region and a variable (V) region. If antibodies are destined to become tethered to the surface of a T-cell membrane (see Figure 6), they are expressed with a transmembrane domain which allows for interaction with membranes. If antibodies are destined to be secreted, the C-terminus of the antibody molecule is assembled lacking a transmembrane domain structure. For both the tethered and secreted forms of antibodies, the variable region (i.e., the fork of the “Y” domain) represents the strategy which animals use to specifically target a unique antigen.

Whether antibodies are tethered or secreted, the constant region may be assembled from distinct genes that in turn yield different antibody isotopes, such as IgG, IgM, IgD, IgA and IgE. Each of these isotopes has different physical properties and different functions in the animal’s body. IgM is the first immunoglobulin isotope to be expressed during B-cell development, and although IgM is an early responder, it has a low affinity against antigen compared to the IgG isotopes. IgG antibodies consist of four subclasses — IgG1, IgG2, IgG3 and IgG4 — and are named in order of abundance in serum.

Relationship of the Innate and Acquired Immune Systems

Initially it was thought that the innate and acquired immune systems functioned independently. However, it is now known that these two arms communicate with one another, and to some extent, rely on similar communication molecules such as interleukin 1B. This molecule, for example, is released by neutrophils when activated by invading pathogens. This stimulates the acquired immune system as a feed- forward system to start the process for antibody production.

Summary

The immune system provides protection from infections and disease-causing organisms. First and immediate response to pathogens is the responsibility of a specific group of white blood cells (macrophages and neutrophils) that comprise a portion of the innate immune system. These leucocytes continually monitor for sites of infection and provide protection until the cow can mount an antibody response.

The adaptive or antibody mediated immune system, which is a pathogen- specific immune response, involves the formation of antibodies. T- and B-cells are cells of the adaptive immune system responsible for the production of antibodies that provide long-term protection against numerous types of pathogens and other disease-causing agents.

A Cow’s Healthy Immune System Starts with Good Nutrition

Good herd health starts with good nutrition, and good nutrition is required to help maintain
a healthy immune system in dairy cows.

When cows are under stress from the strains of production and reproduction, or molds
and mycotoxins in feed and pathogens in the environment, their natural immune system goes to work fighting off those challenges. In an ongoing fight, the cow’s immune system itself can begin to weaken.

That’s why good nutrition is so important, including sufficient energy, fiber, vitamins, trace minerals and the special nutritional supplements your nutritionist or veterinarian may recommend.

Figure 3. Toll-like receptors in cells. Eleven toll-like receptors have been identified and each
binds to a specific PAMP. Toll-like receptors 2 and 4 are responsible for identifying common molds as foreign.

Figure 4. Neutrophil migration/phagocytosis (Janeway, 2005, pg 13)

Figure 5. Cellular interactions involved in induction of immune responses. Activation and proliferation of TII cells (a) is required for generation of a humoral response (b) and a cell response to altered self-cells (c). APC = antigen- presenting cell; Ag = antigen.

Figure 6. Antibody configuration (Janeway 2005, pg 17, figure 1.16)

Aspergillus fumigatus – A Threat to Healthy Cows

Aspergillus fumigatus – A Threat to Healthy Cows

D.L. O’Conner M.S. and J.D. Chapman Ph.D., Dairy Technology Managers, Phibro Animal Health Corporation

Mycotoxins Impact Animal Health and Performance:

Many livestock Introduction producers are aware of the common problems associated with molds and mycotoxins. In general, several species of molds {Aspergillus, Fusarium, and Penicilium) are known to produce common mycotoxins (aflatoxin, zearalenone, trichothecenes, vomitoxin and fumonisin) when growing conditions are adequate (organic nutrient source, temperatures ranging from 23 to 140°F, moisture levels >70%, pH 4-7 and oxygen >0.05%). These mycotoxins, or secondary metabolites of molds, may contribute to losses in performance, reduced growth rate, feed refusal, diarrhea, irregular estrous cycles, abortion, interference with disease resistance and immune function, and vomiting in various livestock species (CAST, 2003).

While there is considerable information in the public domain on the impact of mycotoxins on animal performance, until recently, little emphasis has been placed on understanding the direct effect that certain mold species may have on the development of mycoses or mold-related health disorders in livestock. Much of this knowledge has come from the on-going investigation of the link between Hemorrhagic Bowel Syndrome (HBS), immunosuppression and the mold, Aspergillus fumigatus (AF).

The Dominant Infecting Fungus in Livestock

Aspergillus fumigatus (AF) is a ubiquitous, fast-growing, saprophytic fungus that sporulates abundantly, releasing thousands of airborne conidia from each conidial head. All humans inhale several hundred AF conidia per day.

Healthy people and animals rarely show adverse effects as the conidia are eliminated by the actions of the innate immune system (Latge, 1999). Immunosuppressed people are much more susceptible to invasive aspergillosis as a result of failure of the immune system to reduce and eliminate the pathogenic effect of the conidia. There has been a 14-fold increase in human aspergillosis over the past 15 years as a result of increased use of immunosuppressive therapies associated with cancer, AIDS and organ-transplant therapies (TIGR website; Latge, 1999).

Aspergillus fumigatus and aspergillosis can affect animals as well. It is the dominant infecting fungus in ruminant livestock (Jensen, 1989). Common entry points into the animal are the lungs and the gastrointestinal tract. In ruminants, AF may enter the GI tract at the omasum and Peyer’s Patch immune tissue. Placentitis and pneumonia are secondary infections occurring as a result of the spread of AF through the blood from the primary gastrointestinal lesions. Aspergillosis can account for up to 20% of bovine abortions (Sarfati, et. al., 1996). McCausland, et.al., 1987, reported a 78% incidence of Aspergillus fungal hyphae in the placentas of aborted cattle, with abortions occurring between 6 and 8 months of gestation. Puntenney, et. al., 2003, found a high degree of correlation between the incidence of AF infections and HBS with the bleeding into the jejunum resembling observations in humans infected with AF. Sockett, et. al., 2004, has also reported a high degree of correlation between the incidence of HBS and the presence of AF.

The pathogenicity of AF is attributed to three primary virulence factors. Aspergillus fumigatus produces compounds called siderophores which compete with iron-binding proteins to steal iron from normal biological functions in the host to support fungal growth. The fungus also contains specific types of lipid compounds as cellular constituents which allow fungal organisms to effectively evade the immune system by inhibiting specific pathways responsible for activation of

the complement and phagocytic defense mechanisms. Thirdly, AF produces proteases which facilitate the penetration of fungal hyphae from the site of infection (lungs, GI tract) to the surrounding tissues (Rhodes, et. al., 1992).

Cows Inhale, Ingest Aspergillus fumigatus Conidia

Aspergillus infections start with the inhalation or consumption of AF conidia. These infections become invasive with the activation of the conidia to a hyphal form which initiates active destruction of tissue in the lungs and gastrointestinal tract and movement of the fungus into surrounding tissue (Stanzi, et. al., 2005).

In healthy humans and animals, the innate immune system eliminates Aspergillus conidia, primarily through the actions of phagocytic cells, macrophages and neutrophils. Macrophages and neutrophils recognize, bind, internalize and ingest AF conidia, leading to elimination of the pathogen from the system. Neutrophils also kill hyphae by oxidative mechanisms (ROS or Reactive Oxygen Species) (Svirshchevskaya, et. al., 2003).

The presence of AF conidia or hyphae initiates cytokine or signaling-response mechanisms via IL-1, IL-8, TNF alpha and IL-6 as well as other cytokines. These cytokines serve as an attractant to draw neutrophils to the site of infection and initiate phagocytosis of the fungal organisms (Svirshchevskaya, et. al., 2003).

Innate Immune System Defends Against Aspergillus In immunocompromised humans or animals, innate immune mechanisms fail to function properly to contain the fungal infection. In addition to the virulence factors described earlier which allow the organism to evade destruction and elimination from the body, AF in the hyphal form also produces a mycotoxin called gliotoxin. Gliotoxin has been shown to induce apoptosis (cell death) of lymphocytes and macrophages (Zhou, et. al., 2000). Gliotoxin has also been shown to go through a redox cycle, generating ROS which damage healthy cells in the organs of the host (Zhou, et. al., 2000). Stanzi, et. al., 2005, also demonstrated that gliotoxin interfered with the generation and activation of Tlymphocytes. Low levels of gliotoxin target and kill antigen-presenting cells (monocytes and dendritic cells), resulting in impaired antigen presentation. Reduced or impaired antigen presentation could result in reduced antibody production and impaired adaptive immune system response to viruses, bacteria or vaccines.

Aspergillus fumigatus Prevalence Advances

Aspergillus fumigatus has been detected in a variety of feeds, forages and in the blood and tissues of dairy cows throughout the United States. In 2003, the Department of Animal Sciences at Oregon State University began offering testing of feeds, blood and tissues for the presence of AF DNA. The method used involves analysis of fungal DNA based upon the DNA sequences located within a number of unique regions of the AF genome. To date, it is the only quantitative assessment of AF commercially available. Over 1200 blood samples have been analyzed and 44% of these have tested positive (Table 1).

Texas Survey Shows High Spore Lands in Trench Silos

Additionally, in 2006, a survey was conducted in the dairy sheds of Texas and eastern New Mexico to determine the presence of AF in corn silage, alfalfa silage and small grain silages. Dairies where the feed samples were collected ranged in size from 350 to 4,000 head. All dairies had a previous history of HBS. As expected, the highest level of spore counts came from the top 4 to 12 inches of pile or trench silos, with the lowest coming from the exposed face. Aspergillus fumigatus spore levels ranged from 7,000 to over 990 million spores per gram, averaging 135 million spores per gram of silage (Table 2) (Rickels, 2006).

Aspergillus Image 2Limit Exposure to Aspergillus through Silo Management

Following best management practices for proper storage and rotation of feed ingredients and ensiled forages is paramount to reducing exposure to AF growth. A. fumigatus is extremely tolerant of wide ranges in temperature, 20 to 50°C (68 – 122°F), and grows best in dry, hot conditions. Moisture content should fall between 68-72% for corn silage and between 64-68% for legume haylages going into bunker or drive-over silos. Silage pits should be rapidly filled and immediately packed for best results. Corn silages should reach a pH of 4.0 or less and legume forages should reach a pH below 4.5 for proper fermentation to occur. Bunker silos should be immediately and effectively covered to reduce exposure to air. The spoiled layer at the top of the silo should be carefully discarded. Water troughs and feed bunks should be cleaned regularly to reduce the potential for explosive mold growth (Puntenney, 2003).

Strong Immune System the Best Defense

Building the immune system is also another strategy to allow the dairy cow to effectively deal with the immune challenges associated with the inhalation or consumption of A. fumigatus. Recent studies have measured significant changes in the expression of several immune markers associated with neutrophil migration and phagocytic activity when diets are supplemented with specific nutritional compounds. Wang, et. al. reported a significant change in immune status in ruminants fed these specific nutritional components as measured by L-selectin, a neutrophil- adhesion molecule responsible for movement of neutrophils into tissue being attacked by pathogen (Wang, et. al., 2004; Wang et. al., 2005).

Recently, Forsberg et. al., measured dramatic changes in three neutrophil killing mechanisms when these specific nutritional components were included in the diet of ruminants. These killing mechanisms are associated with a 65% (p<0.01) change in phagocytotic activity, a two-fold (p<0.01) change in ROS or neutrophil respiratory burst activity and a significant difference (p<0.05) in DNA NET extrusion (Forsberg et. al., 2007). Neutrophil killing mechanisms are necessary for the dairy cow’s immune system to recognize, trap and destroy pathogens, such as A. fumigatus, bacteria or viruses.

Changing the activity of these immune mechanisms will impact individual cow health and overall herd productivity and profitability.

A Cow’s Healthy Immune System Starts with Good Nutrition

Good herd health starts with good nutrition, and good nutrition is required to help maintain a healthy immune system in dairy cows.

When cows are under stress from the strains of production and reproduction, or molds and mycotoxins in feed and pathogens in the environment, their natural immune system goes to work fighting off those challenges. In an ongoing fight, the cow’s immune system itself can begin to weaken.

That’s why good nutrition is so important, including sufficient energy, fiber, vitamins, trace minerals and the special nutritional supplements your nutritionist or veterinarian may recommend.

Literature Cited

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JenSen, H., b. AAlbAek, A. bASSe, And H. SHoenHeydeR. THe oCCuRRenCe of fungi in bovine TiSSueS in RelATionS To PoRTAlS of enTRy And enviRonMenTAl fACToRS. J. CoMP. PATH. 107:127- 140. 1992.

lATge, J.P. Aspergillus fumigAtus And ASPeRgilloSiS. CliniCAl MiCRobiology RevieWS. 12: 310-350. 1999.

MCCAuSlAnd, i.P., k.J. Slee And f.S. HiRST. MyCoTiC AboRTion in CATTle. AuST. veT. J. 84:129-132. 1987.

PunTenney, S.b. liMiTing exPoSuRe To A. fumigAtus fRoM iMPRoPeRly enSiled foRAge. oMnigen ReSeARCH uPdATe. vol.1, iSSue 4. 2003.

PunTenney, S.b., y.-Q. WAng, n.e. foRSbeRg. MyCoTiC infeCTionS in liveSToCk: ReCenT inSigHTS And STudieS on eTiology, diAgnoSTiCS And PRevenTion of HeMoRRHAgiC boWel SyndRoMe. PRoC. S.W. AniM. nuTR. MAnAg. Conf. 46-62. 2003.

RiCkelS, J. SuRvey SHoWS HeAlTH-RelATed diSoRdeRS in SouTHWeST CATTle ARe due To A. fumigAtus Mold in SPoiled SilAge. Phibro Animal Health Corporation AdvAnCeMenT. MS170906. 2006.

RHodeS, J., H. JenSen, A. niliuS, C. CHiTAMbAR, S. fARMeR, R. WASHbuRn, P. STeele, And T. AMlung. Aspergillus And ASPeRgilloSiS. J. Med. veT. MyCol. 30:51-57. 1992.

SARfATi, J. H. JenSen, And J. lATge. RouTe of infeCTionS of bovine ASPeRgilloSiS. J. Med. veT. MyCol. 34: 379-383. 1996.

SoCkeTT, d.C. HeMoRRHAgiC boWel SyndRoMe. PRoC 2nd Mid-ATlAnTiC nuTR. Conf., bAlTiMoRe, 2004.

STAnzi, M., e. oRCiuolo, R. leWiS, d.P. konToyiAnniS, S.l.R. MARTinS, l.S ST. JoHn, And kv. koMAnduRi. Aspergillus fumigAtus SuPPReSSeS THe HuMAn CellulAR iMMune ReSPonSe viA glioToxin-MediATed APoPToSiS of MonoCyTeS. blood. 105:2258-2265. 2005

SviRSHCHevSkAyA, e.v. And v.P. kuRuP. iMMunoTHeRAPy of AlleRgiC bRonCHoPulMonARy ASPeRgilloSiS: A CliniCAl exPeRiMenTAl APPRoACH. fRonTieRS in bioSCienCe: 8:92-101. 2003.

vAn MeTRe, d. Phibro SuMMiT, 2005.

WAng, y.-Q., S.b. PunTenney, And n.e. foRSbeRg. idenTifiCATion of THe MeCHAniSMS by WHiCH oMnigen-Af, A nuTRiTionAl SuPPleMenT, AugMenTS iMMune funCTion in RuMinAnT liveSToCk. PRoC. WeSTeRn SeCTion. ASAS, vol. 55: 2004.

WAng, y.-Q, J.l. buRTon, And n.e. foRSbeRg. MiCRoARRAy AnAlySiS of THe iMMunoRegulAToRy ACTionS of oMnigen-Af in PeRiPARTuRienT dAiRy CATTle. J. dAiRy SCi., vol. 88, SuPPl. 1, P.220, 2005

zHou, x., A. zHAo, g. goPing, And P. HiRSzel. glioToxin-induCed CyToToxiCiTy PRoCeedS viA APoPToSiS And iS MediATed by CASPASeS And ReACTive oxygen SPeCieS in llC-Pk1 CellS. ToxilogiCAl SCienCeS: 54:194-202. 2000.

HTTP://WWW.TigR.oRg/Tdb/e2k1/Afu1/inTRo.SHTMl

Figure 1.

1 = conidiophore
2 = hypha
3 = conidia
4 = germinating conidium

Hemorrhagic bowel syndrome in a dairy cow. (Van Metre, 2005)

Table 1: Summary: results from blood samples submitted for A. fumigatus (AF) DNA testing by region.

A. fumigatus DNA determined by real-time PCR by Oregon State University, Immunobiology Laboratory. Traces: levels periodically detected in cattle, generally not of concern (0-1 GU x 104/ml). Positive: cattle in upper 25 percentile of AF levels detected in cattle, and may be cause of concern (1-3 GU x 104/ml). Positive +: cattle in the upper 10 percentile of AF levels detected in cattle, and are cause for concern (3->100 GU x 104/ml).

Table 2: A. fumigatus in silage from Texas- New Mexico dairies

a Sample location: Top = 4-12 inches from top layer; Face = across face either by gram or by silage probe; Slab = from loose silage at base; Bag = 4-12 inches from top or side; ns = no sample collected.

Bedding, Bacteria and Environmental Mastitis

Bedding, Bacteria and Environmental Mastitis

J.S. Hogan, ph. d., ohio agricultural research and development Center, the ohio State University; Wooster, ohio.

Introduction

The American Heritage Dictionary defines environment as “the combination of external physical conditions that affect and influence the growth, development, and survival of an organism or group of organisms”. Relative to bovine mastitis, the environment influences both of the principal groups of participants: bacteria and cows.

Specifically, environmental conditions will affect the rate and magnitude of bacterial growth in the cows’ surroundings. The other primary factor determining the incidence of environmental mastitis is the mammary glandhostdefenses.Thesameenvironmental factors that increase the growth of common mastitis pathogens often have a negative effect on mammary defenses.

The Bacteria’s View

The primary environmental mastitis pathogens include Escherichia coli, Klebsiella pneumonia, and Streptococcus uberis. These bacterial species require organic material to utilize as food. Bedding materials commonly used for lactating and nonlactating cows provide an excellent environment for propagation of mastitis pathogens.

Populations of the bacteria in bedding are related to the number of bacteria on teat ends and rates of clinical mastitis. Therefore, reducing the number of bacteria in bedding generally results in a decrease in environmental mastitis.

Coliforms and streptococci cannot live on teat skin for long periods of time. If these bacteria are present in large numbers on teat skin, it is the result of recent contamination from a source such as bedding. Thus, the number of these bacteria on teat skin is a reflection of the cow’s exposure to the contaminating environment.

One of the environmental factors that has the greatest impact on bacteria in the cows’ surrounding is the choice of bedding materials. The bacterial view of life apparently is very simple: eat, drink, and reproduce. Unfortunately, many materials used to bed dairy cows allow

for bacteria to accomplish these meager goals with astounding proficiency. Many organic materials provide adequate nutrition for both coliforms and environmental streptococci to reach populations in excess of 10 million colony forming units per gram of bedding.

Common organic bedding materials such as sawdust and straw usually contain very few mastitis pathogens before use as bedding. However, mastitis pathogens that contaminate the cows’ environment establish residence in the bedding and often reach maximum populations within 24 hours after fresh bedding is added to stalls. The rapid increase in bacterial populations often preclude the soiled appearance of bedding. Therefore, the gross appearance of bedding has little correlation with bacterial load.

Bacterial populations tend to remain constant for up to 7-to-10 days, then start to decline due to the exhaustion of nutrients in bedding. The common practice of adding “fresh” bedding to stalls or manure packs replenishes the essential nutrients and maintains bacterial populations.

Particle size of bedding influences bacterial populations. Finely chopped materials support greater bacterial numbers than the same bedding with larger particlesizes. Finely chopped organic material has greater surface area for attachment and colonization by bacteria.

For example, chopped straw generally has higher counts than long straw, sawdust greater than shavings, and chopped newspaper greater than shredded paper. In addition, finely chopped materials adhere more readily to teat skin than larger materials, thus increasing exposure of the teat end to mastitis pathogens.

Growth rates of coliforms and environmental streptococci are greatest during warm, wet weather. The effects of season on bacterial populations in bedding are quite dramatic in regions that experience a wide variation of temperatures within a year. In general, the impact of bedding on exposure of cows in confinement housing decreases during cold weather and increases as temperatures and humidity increase.

Previous trials have shown a strong correlation between bacterial counts in bedding and both ambient temperature and relative humidity. Therefore, proper ventilation of barns is essential to moderate the effects of heat and humidity in housing areas.

Climatic factors affecting exposure in herds where cows are maintained on dry lots differ from those of traditional Midwestern and Eastern herds. Dry lots are used primarily in hot, arid areas where temperatures are seldom

below freezing for an extended time. In these areas, the rainy seasons of late Fall through early Spring are when bacterial populations are greatest. Manure in dry lots during the Summer tends to be desiccated, thus limiting the moisture essential for bacterial growth.

The Cow’s View

Much like bacteria, the primary goals of a cow are to eat, drink, and to continue propagation of the species. The latter of these is an environmental factor that greatly affects the incidence of mastitis.

Parturition, lactation, mammary involution, and lactogenesis (initiation of milk secretion) are each reproductive events that influence the susceptibility of the mammary gland to infection. Rates of new intramammary infections caused by environmental streptococci and coliforms are greater during the dry period than during lactation. During the dry period, susceptibility to intramammary infection is greatest the two weeks after drying off and the two weeks prior to calving.

Many infections acquired during the dry period persist to lactation and become clinical cases. Research has shown that 65% of coliform clinical cases that occur in the first two months of lactation are from intramammary infections (IMI) that originated during the dry period.

Streptococcal infections during the dry period account for 56% of clinical cases during the first two months after calving. Rate of

intramammary infections during lactation is highest at calving and decreases as days in milk advances. (Figure 1.)

Therefore, the thrust of herd management strategies for controlling environmental mastitis should focus on reducing intramammary infections during the dry period and early lactation.

Housing and other environmental concerns for dry and maternity cows often are precluded by the comfort and housing needs of lactating cows. However, given the impact of intramammary infections acquired during the dry period on the subsequent lactation, providing cows with a clean and dry environment is not limited to during lactation.

Dry cow and maternity facilities should be managed similar to lactating cow housing. Dry cow areas should be well drained and free of excess manure. Dirt covered areas can expose cows to pathogen levels comparable to those in free stalls. Box stalls and loose housing areas should be cleaned to the foundation base regularly. Manure packs are to be avoided because they generally contain extremely high counts of pathogens dangerous to both dam and calf.

Bedding Management

The bedding material that we recommend most for controlling environmental mastitis is washed sand. Ideally, bedding should be inorganic materials that are low in moisture content and contain few nutrients for bacteria to utilize.

Washed sand has little nutritive value to common mastitis pathogens, thus limiting their growth. Washed sand consistently contains fewer mastitis pathogens compared with organic materials such as sawdust, recycled manure, straw, and dirt.

On-farm separation sand from manure by mechanical devices or passive settling in ponds has gained popularity as a means to reduce hauling charges and allow the recycling of sand. Care must be taken to assure the reclaimed sand has minimal organic contamination. A rule of thumb is the ash content of sand (estimate of organic load) should be below 3% for use as dairy cow bedding.

Many free stall barns are forced to use organic bedding materials that are compatible with liquid manure handling systems. There appears to be little advantage in using one organic material over the use of another.

For example, straw tends to have highest streptococcal counts, while sawdust and recycled manure have highest coliform counts in comparisons among these bedding materials.

Recycled manure bedding has regained popularity as dairies strive to be more ecologically responsible by separating manure solids and installing methane digesters. Recycled manure solids often have bacteriological properties similar to those of sawdust when used as bedding. Composting and heating recycled manure and sawdust can initially reduce bacterial populations before use as bedding, however these treatments have minimal effect on reducing teat end exposure after 24 hours in free stalls.

Any material to be used as bedding should be stored in a dry area to prevent saturation by rain and ground moisture. Composting organic materials such as manure is an effective way to reduce bacterial counts before use as bedding. However, although many organic bedding materials have relatively few mastitis pathogens prior to use, the pathogen populations often increase 10,000-fold within a few hours when used as bedding.

Fresh bedding tends to absorb moisture from the cows’ environment for use by the great number of bacteria that are constantly present in manure and soiled bedding.

Regardless of the bedding used, removing wet and soiled material from the back one- third of stalls will significantly reduce the bacterial counts. Stalls should be raked a minimum of twice daily when animals are moved to be milked. Spraying bedding with disinfectant and adding powdered lime or conditioners to bedding have met with little practical success in reducing bacterial counts.

These practices cause an initial decline in bacterial populations, but pathogen numbers quickly recover. Twice a day application of powdered lime may be necessary to sustain

an advantage in lowering bacterial numbers. Avoid standing water and mud in free stalls, holding areas, and corrals.

Dirt and manure covered corrals are commonly used to house cows in semi-arid and arid areas. Exposure to pathogens generally is low during the dry seasons as moisture content of the dirt- manure mixture is low.

However, as density of cows increase under shade structures and around feeding areas and water troughs, excess wet organic matter should be removed or spread out to be dried. Cows’ access to dirt-manure lots should be limited during rainy seasons. Outbreaks of coliform mastitis are common during rainy seasons when cows are exposed to dirt-manure lots and alleys leading to the milking parlors.

Conclusions

An old, but popular, mastitis cliche is that environmental mastitis control is based on keeping cows clean, dry and comfortable. While this is true, the other half of the mastitis equation must also be accounted. Mastitis pathogens must be kept cold, thirsty and hungry.

Engineering decisions and husbandry practices should consider the importance of maintaining cow comfort and a healthy immune system while simultaneously minimizing pathogen populations in the environment.

Figure 1. sizes. Finely chopped organic material has greater surface area for attachment and colonization by bacteria.

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