Polioencephalomalacia Investigations

Illustration showing the occurrence of polioencephalomalacia related to high sulfate water


Polioencephalomalacia (PEM) is an important neurological disease of ruminants seen worldwide. It is characterized by degeneration of the cerebral cortex that results in visual, behavioral, and motor disturbances, hence the common name “blind staggers”. Historically PEM has been associated with disturbances in thiamine status. This was based on studies of a few naturally occurring cases of PEM, as well as the beneficial effect that treatment with thiamine has on PEM cases. Some investigators reported cases that seemed to be associated with elevated levels of sulfate in feed. In fact, in Colorado we observed PEM ranch outbreaks associated with water sources high in sulfate salts.

Occurrence of PEM related to high sulfate water (right).

To make progress in understanding the etiology of PEM it was necessary to unravel the relationship thiamine status and dietary sulfur.

Experimental and field investigations

Our work in Colorado began with an unexpected finding in experiments designed to study the effects of copper (Cu) deficiency in cattle. The deficiency-inducing diet was high in carbohydrates and sodium sulfate and low in fiber. As feeding period progressed some calves developed PEM. With this as possible model of PEM, the research was shifted to explore the pathogenesis of the neurological disease.

The first experiment was to assess whether copper deficiency or decreased thiamine was associated with PEM. Neither alteration was observed in the calves that developed PEM (Sager, 1990). During this experiment, the fleeting odor of H2S was occasionally detected on the breath of calves developing PEM.

The next set experiments demonstrated that calves with nutritionally-induced PEM had normal levels of thiamine and all its derivates in blood, cerebrospinal fluid, brain and liver. Furthermore, elevated concentrations of sulfide anion were measured in rumen fluid of affected calves (Gould, 1991) (supported by U.S. Department of Agriculture, Special Competitive Research Grants Program 1987-1990). Based on the demonstration of elevated rumen sulfide in PEM affected calves, sulfur-reducing bacteria (SRB) in the rumen were evaluated by a variety of methods. It was shown that sulfide production was not associated with elevated SRB numbers, but by sulfide-generating activity that increased with time of exposure to high sulfur substrate. (Cummings, 1995a, 1995b) (U.S. Department of Agriculture, National Research Initiative Competitive Grants Program 1991-1993)

A field study at a large feedlot with seasonal occurrences of PEM associated with a high sulfate water source showed that rumen sulfide concentrations peaked at 30 days after entry to the feedlot and was followed by decreased sulfide production. The peak incidence of PEM cases coincided with the peak in rumen sulfide production. Since cattle with clinical PEM go off-feed, rumen sulfide concentration quickly declines after the onset of signs. Elevated levels are detectable only in very early PEM cases or in clinically normal pen mates still consuming the high sulfate water. Thiamine concentrations in affected and normal cattle in the feedlot were within the normal range (McAllister, 1997).

A better understanding of how sulfur-associated PEM develops would be possible if rumen gas cap H2S could be measured, rather than the sulfide content of rumen fluid. Because eructated gas in efficiently absorbed via inhalation, the dynamics of ruminal gas cap H2S could be more relevant to the induction of PEM. To do this a precision volumetric gas pump was used to draw a gas cap sample via a percutaneous 18-gauge needle through a calibrated H2S detector tube. The method was validated by comparison to standard analytical methods. This proved to be a convenient method to study sequential changes in H2S production and their relation to the onset of clinical signs (Gould, 1997).

This new technique proved useful in a field study of a naturally occurring PEM outbreak in a group of weaned beef calves. After the diagnosis of PEM was established in the affected calves brought to the veterinary hospital for treatment and/or necropsy, ruminal gas cap H2S was assessed in the clinically normal herd-mates. All calves had markedly elevated levels of gas cap H2S, and 2 calves with the highest levels developed clinical signs of PEM the day after sampling. All the calves with excessive (pathologic) gas cap H2S had normal blood thiamine levels, even the ones that developed signs of PEM. Analysis of the diet of these calves revealed high levels of sulfate in the water, in the grass hay and in the Canada thistle contaminating the hay (Loneragan, 1998)

The relationship of PEM and pathologic ruminal H2S production was presented at a symposium on “Metabolic Disorders of Feedlot Cattle” (Gould, 1998). An updated review of sulfur-associated PEM along with various combinations of dietary conditions observed in field outbreaks of PEM was presented in an invited paper (Gould, 2000). In a cross-sectional study of water and forage resources in geographically diverse cow-calf operations, the potential for pathologic rumen sulfide generation was evaluated. Eleven percent of the water-forage pairs could, under conditions of high ambient temperature, result in a total dietary sulfur level ³ 0.4%, which is a hazardous situation. Most of these operations were in north-central or western states (Gould, 2001).

The effects of various water sulfate concentrations up to 2400 ppm were studied in feedlot cattle. Changes in performance, water intake and carcass characteristics were evaluated. Water sulfate concentrations greater than 580 ppm decreased feedlot performance (Loneragan, 2001). More detailed studies of the effects of high sulfate water in feedlot cattle revealed changes in magnitude and pattern of rumen gas cap H2S concentrations. Serial sampling showed the H2S levels increased and peaked between days 15 and 31 on feed. One calf in the test group (N=27) developed clinical signs of PEM during the peaking period. In a larger population of feedlot cattle fed under the same environmental and dietary conditions, peak numbers of PEM cases occurred in a temporal pattern similar to the measured H2S peaking pattern observed in the test group. In addition, blood thiamine concentrations in the test group were measured at different time points to detect an effects of H2S generation on thiamine status. Thiamine status was unaffected (Loneragan, 2005).


These investigations have shown that sulfur-associated PEM is a distinct form of the disease. It is characterized by pathologic ruminal sulfide generation. In order to mitigate and/or prevent the disease it is necessary to identify the source or sources of sulfur in the diet. With such knowledge, the safe use of valuable, but potentially high sulfur, dietary components is possible (e.g., biofuels co-products [distiller’s grains], oil seed crops and cruciferous forages).


  • Sager RL, Hamar DW, Gould DH: Clinical and biochemical alterations in calves with nutritionally induced polioencephalomalacia.  Amer J Vet Res 51:1969-1974, 1990.
    Gould DH, McAllister MM, Savage JC, Hamar DW:  High sulfide concentrations in rumen fluid associated with nutritionally induced polioencephalomalacia in calves.  Amer J Vet Res 52:1164-1169, 1991.
  • Cummings BA, Caldwell DR, Gould DH, Hamar DW:  Identity and interactions of rumen microbes associated with dietary sulfate-induced polioencephalomalacia in cattle. Am J Vet Res. 56:1384-1389, 1995a
  • Cummings BA, Gould DH, Caldwell DR, Hamar DW: Rumen microbial alterations associated with sulfide generation in steers with dietary sulfate-induced polioencephalomalacia. Am J Vet Res. 56:1390-1395, 1995b
  • Gould DH, Cummings BA, Hamar DW; In vivo indicators of pathologic ruminal sulfide production in steers with diet-induced polioencephalomalacia, J Vet Diag Invest, 9:72-76, 1997
    McAllister MM, Gould DH, Raisbeck MF, Cummings BA, Loneragan GH:  Evaluation of ruminal sulfide concentrations and seasonal outbreaks of polioencephalomalacia in beef cattle in a feedlot. J Amer Vet Med Assoc 211:1275-1279, 1997
  • Gould DH, Symposium: “Bud Britton Memorial Symposium on Metabolic Disorders of Feedlot Cattle”.   Polioencephalomalacia, J. Anim. Sci. 76:309-314, 1998
    Loneragan GH, Gould DH, Callan RJ, Sigurdson CJ, Hamar DW: Association of excess total sulfur intake and an increase in H2S concentrations in the ruminal gas cap in recently weaned beef calves with polioencephalomalacia.  J Amer Vet Med Assoc 213:1599-1604, 1998
  • Gould, DH: Update on sulfur-associated polioencephalomalacia. Veterinary Clinics of North America: Food Animal Practice, Toxicology. 16:481-496, 2000 (invited review)
    Loneragan GH, Wagner JJ, Gould DH, Garry FB, Thoren MA. Effects of water sulfate concentration on performance, water intake, and carcass characteristics of feedlot steers.  J Anim Sci 79:2941-8, 2001
  • Gould DH, Dargatz DA, Garry FB, Hamar DW, Ross PF:  Potentially hazardous sulfur conditions on beef cattle ranches in the United States. J Amer Vet Med Assoc 221:673-677, 2002
    Loneragan GH, Gould DH, Wagner JJ, Garry FB, Thoren MA. The magnitude and patterns of hydrogen sulfide production, blood thiamine concentration, and mean pulmonary arterial pressure in feedlot steers consuming water of different sulfate concentrations. Bov Pract 39(1):16-22. 2005