J.K. Underwood and coworkers in Tennessee intuitively noted that the animal signs were similar to those of ergotism but they eliminated this possibility because there were no ergot sclerotia [Claviceps purpurea (Fr.:Fr.) Tul.] in tall fescue seedheads (unpublished, 1954, as related to H.A. Fribourg). Surprisingly, this clue was not pursued, perhaps because such unfavorable news might hinder sales of tall fescue seed grown by some producers (personal communication, 2001, H.A. Fribourg, as related to him by the late J.B. McLaren in 1990). Instead, research was concentrated on external plant fungi, plant alkaloids, toxins produced in the rumen, and anions during the 1950s to 1970s (Bush et al., 1979). Of the many alkaloids found in tall fescue, perloline was thought to be a major factor, and a breeding program in Kentucky developed low-perloline lines. Unfortunately, low-perloline tall fescue was no more successful than other approaches in solving the toxicosis problem.
For several years, Dr. J.D. Robbins, a toxicologist at the USDA Russell Research Center in Athens, GA, had become convinced that tall fescue toxicity involved a fungus because the symptoms were similar to those from ergot toxicity (Robbins, 1983). In 1973, Robbins and his associates C.W. Bacon and J.K. Porter isolated three species of Balansia fungi from a toxic tall fescue pasture in north central Georgia (Bacon et al., 1975). These fungi were endophytic (i.e., they live within the host plant) and not virulent to their grass host. This group of fungi was first associated with grass toxicosis of cattle and goats (Capra spp.) in India (Nobindro, 1934). Toxicological studies demonstrated these endophytic fungal species in Georgia were toxic to animals and had the potential for ergot alkaloid synthesis (Porter et al., 1979). These findings resulted in the hypothesis that an endophyte was the causal agent in fescue toxicosis and stimulated further research (Bacon, 1995). Later, these scientists became aware of research by Neil (1941) in New Zealand that confirmed a fungal endophyte in tall fescue and perennial ryegrass, suspecting that it might produce a toxic compound. The first discovery of a grass endophyte was reported in 1898 by Vogl in Germany (White et al., 1993). The dependence of the endophyte on seed transmission for dispersal was demonstrated by Sampson (1933) in Wales.
The role of the U.S. federal bureaucracy adds an interesting aspect to this story. On June 13, 1973, J.D. Robbins visited the A.E. Hays farm near Mansfield, GA and observed severe fescue toxicosis signs on beef cattle in one tall fescue pasture but none in three adjacent pastures of this grass (Robbins, 1983). Reporting this exciting find to his laboratory chief at the Russell Research Center, he requested permission to return and sample the pastures for fungal endophytes but was denied leave to travel, as apparently this was not considered a worthwhile pursuit (correspondence from J.A. Robertson to D. Burdick, with copy to J.D. Robbins, 1973). The next day he departed without official leave in his personal vehicle and sampled the pastures on the Hays farm. C.W. Bacon, mycologist at the Russell Center, examined plant tissue samples from these pastures under the microscope and found that 100% of the plants in pastures with cattle showing toxicosis symptoms were infected with the fungal endophyte Epichloë typhina (Pers., Fr.) Tul. [renamed Acremonium coenophialum Morgan-Jones and Gams and later Neotyphodium coenophialum (Morgan-Jones and Gams) Glenn, Bacon, and Hanlin], while the pastures with cattle in good condition had a much lower infestation rate (Bacon et al., 1977). This was very strong circumstantial evidence suggesting the fungal endophyte was the probable cause of toxicosis.
Further evidence of the association between endophyte and fescue toxicity came from a 3-yr grazing trial in central Alabama in which paddocks with only 18% endophyte infestation resulted in 51% higher steer average daily gain (ADG) than in a paddock with 80% infestation (Hoveland et al., 1980). The final confirmation of the fungal endophyte as the causal agent of toxicosis came from a central Alabama grazing trial with three replications in a 4-yr period (Hoveland et al., 1983). Steer ADG was 66% greater and gain per acre was 28% greater in tall fescue paddocks with 5% infestation as compared with those having 94% endophyte infestation (Fig. 1-2). Steers on the heavily infested tall fescue had typical toxicosis signs: elevated body temperature, rough haircoats that did not shed in spring, excessive salivation, and nervousness. In contrast, steers grazing on the low-endophyte grass were in excellent condition, with slick haircoats, were tolerant of heat, grazed during the day, and exhibited no nervousness.
These findings were dramatic evidence that the fungal endophyte was responsible for the tall fescue toxicosis syndrome. However, that conclusion was not readily accepted by many scientists. Some had spent many years working hard to find the causal agent, so it was difficult to accept that their work had been largely in vain. Admittedly, several problems remained - identifying methods to reduce the toxicity problem, understanding the life cycle, finding the source of the endophyte, characterizing the effect on the host plant, and identifying the toxic product(s).
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|Fig. 1-2. Steers from one of the first experimental comparisons of fungus infested and fungus free tall fescue pastures, Black Belt Experiment Station, Auburn University, AL, about 1978. Left: steer from E- pasture; right: steer from E+ pasture. (Photo by C.S. Hoveland.)|
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