Saprotrophic fungi and bacteria and commensal bacteria that infect frost-damaged pastures may be contributing to gut microbial overgrowth and lesions associated with the mare reproductive loss syndrome

Abstract

The mare reproductive loss syndrome (MRLS) that occurred in 2001 was first recognized as a syndrome of unknown origin responsible for earlyand late-term abortions in 1980 and 1981.1,2 In each of these years, spikes in abortions seemed to be associated with nutritious, high-protein diets, especially lush spring pastures. In each year that MRLS occurred, there were unusual weather conditions. The winter months were drier than normal, followed by periods of extremely warm and cool wet conditions in the spring with late frosts and/or freezes to rapidly growing lush pastures.3 Frosts will induce acute changes in plant electrolytes and minerals4 and will cause sugars to increase in plants.5 The increase in potassium, nitrates, and sugars that occurs in frost-damaged plants may make these plants ideal substrates for fungi. Saprotrophic fungi, like Aspergillus spp, are excellent producers of multiple enzymes that may even further promote the digestion of proteins and carbohydrates, making them more readily available to the gut microflora. These saprotrophic fungi and bacteria are naturally found in decaying soils and pasture plants.6 In the spring, especially after frost damage to lush grass, horses and foals seem to develop episodes of loose feces and diarrhea in more severe cases. This is suggestive of a digestive upset induced by excessive dietary nutrients and/or toxic byproducts of gut microbial overgrowth. Also, sequelae to these digestive upsets may be pericarditis and cardiac effusion, which are commonly seen in fast-growing foals and young horses and are associated with MRLS. Coincidentally, in 2001, cattle herds were also experiencing episodes of very loose feces and severe diarrhea. I investigated 3 of these cattle herds with severe diarrhea that were loosing calves because of pericarditis and cardiac tamponade with no lesions in other organs. In one herd of 55 Angus cows and 55 suckling calves, 18 of the largest and fasting growing calves, weighing approximately 450 to 500 pounds, died. This herd of cattle was grazing lush grass and clover pastures and was being fed a premix feed supplement-free choice. This feed supplement contained 17% sodium chloride and was fortified with essential macroand microminerals, potassium chloride, molasses, and microbial byproducts containing enzymes to enhance plant digestion. According to the owner, cows and calves seemed to be overconsuming the supplement, and all cows and calves had diarrhea. After 18 calves died within a 5-day period, the owner removed the feed supplement from the pasture and replaced it with loose unfortified salt (sodium chloride). No other changes or treatments were made in the herd. Within 24 to 48 hours, the diarrhea in all cows and calves stopped, and there were no more deaths in the herd. Likewise, in other cattle herds with the pericarditis syndrome, all deaths stopped after the addition of readily available loose salt (sodium chloride) to the herd. Recently, in 2002, I investigated another cattle herd of 37 calves on a growing feed and forage ration that was fed in a dry lot. The calves were not exposed to pasture grazing. Calves were given a concentrated enzyme supplement containing enzymes produced by Aspergillus niger, A oryzae, Bacillus spp, and other enzyme-producing saprotrophic organisms. The only change in the diet for several weeks was the addition of this enzyme supplement. Within 2 to 3 days after adding the enzyme supplement to the ration, all calves developed diarrhea, and 1 calf was found dead. Several other calves required extensive supportive therapy but survived. The enzyme supplement was suspected as the cause of the acute digestive upset and was immediately removed from the ration. The diarrhea in all calves stopped within a few days without further treatment. The acute readily available nutrients induced by the enzymes likely caused the gut flora to overgrow and to produce opportunistic pathogens and toxic byproducts. Microaerophilic Streptococcus spp, Actinobacillus spp, Clostridium spp, and other gut opportunistic pathogens are commonly found in fetuses and foals affected with MRLS. In humans, pericarditis with cardiac tamponade is associated with uremia7 and secondary infections with bacteria, like Streptococcus spp and Clostridium spp.8 Similarly all calves that were necropsied in each of the 3 herds with pericarditis and cardiac tamponade were infected with the anaerobic bacterium Clostridium chauvoei, with no other lesions elsewhere in the body. In addition, numerous streptococcal-like bacteria could also be seen in histopathologic lesions in the heart and pericardium. This same type of gut microaerophilic Streptococcus spp is commonly found in equine fetuses and foals affected with MRLS and was first associated with early fetal abortions in 19801 and again in 1981.2 Overgrowth of gut microaerophilic From the Department, College of Agriculture, University of Kentucky, Lexington, KY. Address reprint requests to T. W. Swerczek, DVM, PhD, Copyright 2002, Elsevier Science (USA). All rights reserved. 0737-0806/02/2206-0002$35.00/0 doi:10.1053/jevs.2002.35827