This is how cattle should be on healthy pastures in summer. Unfortunately, grasses are not always healthy for grazing animals .
A condition that is increasingly affecting younger and younger horses is Equine Cushing's Syndrome (ECS). In the past, it was amed that tumors on the pituitary gland in the brain would lead to a disturbance of the hormone level and thus trigger the disease. Since today also horses partly under 8 years are affected, this cause is rather unlikely in all horses. But then what could cause this disease?
Cushing's syndrome is another name for the scientific term hypercortisolism, meaning "too much cortisol all the time". The hormonal cause is a disturbance in hormone levels with significantly excessive cortisol production. Cortisol is an antagonist of insulin. If the body is trying to balance by also constantly raising insulin levels, then the horse has a problem: insulin levels kept too high for 72 hours or more will certainly trigger laminitis in the horse on all four hooves (Asplin et al. 2007). But why is the cortisol level too high?
In experiments on cattle, ergot toxins (ergotamine tartrate) increased cortisol concentrations in blood plasma (Browning et al. 1998b). In cattle, an elevated cortisol concentration is considered a stress indicator. When cattle graze on pastures infected with endophytes and thus containing toxic agents, they are constantly exposed to a mixture of different ergot poisons (ergot alkaloids). Chronic ingestion of endophyte-infected grasses may be a cause of altered glandular tie function with reduced reproduction in cows on appropriate grassland, according to Browning and coworkers (1998a).
If in the USA a cow shows laminitis, i.e. laminitis of the hooves (occurs there in cattle preferentially during frost in winter), is unable to change its winter coat in spring (hirsutism), emaciates, puts itself in the shade or in water, to avoid overheating of the body (cattle have fewer sweat glands than horses and can therefore sweat less to prevent overtemperature, i.e. "fever"), drink and urinate more frequently, and suffer infectious diseases due to a weakened immune system – then this cattle is clearly diagnosed with ergovaline poisoning. But wait – weren't those the symptoms we are told for ECS?
Especially hirsutism, i.e. a coat that is clearly too long and does not want to change in spring or autumn, is supposed to be a clear sign of ECS! The company Boehringer-Ingelheim, which sells the drug Prascend, writes in its information brochure about ECS: "Hirsutism is the only definite symptom. (…) Ca. 20% of horses and ponies over 15 years of age suffer from Equine Cushing Syndrome (ECS)!" Also Dr. Albrecht Fenner of Boehringer-Ingelheim states in a lecture on ECS: "Clearly, hirsutism (hair change disorder to all year round too dense, long and curly hair coat)."(paper published in z. B. in the farrier journal "Der Huf" Nr. 154, 02/2012, S. 26)
A publication by Rosenkrans and colleagues in 2010 should make us horse owners sit up and take notice. It is old textbook wisdom that ergot toxins drastically inhibit the formation of the hormone prolactin in the body. However, prolactin has several functions. It not only ensures the formation of milk in mammals. Deficiency here thus leads to milklessness. Prolactin is also important for the immune system, so deficiency leads to immunodeficiency. Rosenkrans and coworkers now show the importance of prolactin in the formation of hair coat:
Prolactin doses of 4 mg per day for 45 days triggered a strong coat change in mares in experiments by Thompson and coworkers in 1997, cited by Rosenkrans. Rodents react in experiments with increased hair growth. Coat change problems to ergot toxins. In sheep, prolactin receptors are found in the skin papillae. The root sheaths of the wool follicles. Not only in mice (Craven et al. 2006) there seem to be direct correlations between the hair coat. To exist to the prolactin level. In addition, Rosenkrans points out that both prolactin and ergot toxins (ergot alkaloids) directly alter blood vessel width, blood flow, and blood prere. Angiogenesis, i.e. the formation of new blood vessels, is influenced by prolactin.
Since cattle respond to ergot toxin ergovaline of endophytes in grasses with laminitis (Yoder& Fournier 2002) to complete shoeing of the horn capsules (Parsons& Bohnert 2003) can react, I would not expect anything else in horses. In ergot poisoning, massive interruption of blood flow to extremity ends is known to occur. If then also the formation of new blood vessels v. a. is altered in the damaged dermis, then the stressed hoof should have very serious problems.
I have tried to bring the publication of Rosenkrans at the Symposium 2010 to the attention of the German Veterinary Association with its journal "Deutsches Tierarzteblatt". In the reply from the editor-in-chief to me dated 5. August 2014, it says about the reaction of the expert committee: "From there comes the assessment that valid scientific data supporting the presented hypothesis are not available in science and also do not emerge from your article. So publication is definitely out of the question." Here experts are quite divided opinion. Recommend other veterinary journals to reprint the facts presented by Rosenkrans."Here experts are quite divided opinion and recommend other veterinary journals to print the facts presented by Rosenkrans.
Dr. rer. nat. Renate Vanselow, graduate biologist
Among the typical symptoms of grass poisoning is the inability to change the winter coat in spring (unshed haircoat). The effects of hirsutism caused by endophyte toxins acting on the hair coat of cattle can be found in the Tall Fescue online Monograph look at the Oregon State University (USA). The captions of the photos shown there read translated into German: "Fig. 16-1. A gating bull in July 2003 after grazing endophyte-infected (E+) tall fescue since March in Knoxville, TN. Note the unchanged winter coat and unflattering appearance compared to the smooth and shiny coat of the bull in Fig. 16-2." and "Fig. 16-2. An angus animal in July 2003 after grazing endophyte-free (E) tall fescue since March in Knoxville, TN." The bronze-colored lightening often observed, as in the black Angus cattle shown here (Fig. 16-1) with this symptomatology, is generally attributed to pigment disorders caused by copper deficiency (http://forages.oregonstate.edu/tallfescuemonograph/endophyte/soil/copper): Tall fescue infected with endophytes take up less copper from soil than uninfected tall fescue. In addition, grass toxins appear to interfere with the uptake of copper by cattle from the dietary mash. It is suspected that the toxin ergovalin is responsible for this symptomatology of the coat. Ergovaline is produced by both infected tall fescue and infected perennial ryegrass."
Asplin, K. E., M. N. Sillence, C. Pollitt& C. M . McGowan (2007): Induction of laminitis by prolonged hyperinsulinaemia in clinically normal ponies. – The Veterinary Journal, available online Aug. 24.
Browning Jr., R., F. N. Schrick, F. N. Thompson& T. Wakefield Jr. (1998a): Reproductive Hormonal Responses to Ergotamine and Ergonovine in Cows During the Luteal Phase of the Estrous Cycle. – J. Anim. Sci., 76: 1448-1454.
Browning Jr., R., M. L. Leite-Browning, H. M . Smith& T. Wakefield Jr. (1998b): Effect of Ergotamine and Ergonovine on Plasma Concentration of Thyroid Hormones and Cortisol in Cattle. – J. Anim. Sci., 76: 1644-1650.
Craven, A.J., Nixon, A.J., Ashby, A.G., Ormandy, C.J., Blazek, K., Wilkins, R.J. & A.J. Pearson (2006): Prolactin delays hair regrowth in mice. Journal of Endocrinology, 191: 415-425.
Fenner, A. (2011): Hormonally induced laminitis. Detection, treatment and prevention. – 12th International Farrier Forum, Olsberg, Germany, 16.-17. September 2011.
Rosenkrans, C.F., JR, Mays, A.R., Aiken, G.E., & M.L. Looper (2010) 1.6 Prolactin genomics and biology in herbivores. In: C.A. Young, G.E. Aiken, R.L. McCulley, J.R. Strickland, C.L. Schardl (Editors): Epichloae, endophytes of cool season grasses: Implications, utilization and biology.