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Randomized, masked, prospective clinical trial evidence for therapeutic intervention in naturally occurring bovine polioencephalomalacia (polio) is nonexistent. This article evaluates the use of thiamine and anti-inflammatories in the therapy of polioencephalomalacia based on available information related to the pathophysiology of the disease, induced models, disease outcome in other species (sheep), and parallels in similar disease in humans.

This study examined the role of sulfur (S) in the pathogenesis of S-induced polioencephalomalacia (PEM) in beef cattle in the context of thiamine status and metabolism. Thiamine, thiamine monophosphate (TMP) and thiamine pyrophosphate (TPP) status in rumen fluid, blood and brain tissue were determined in beef heifers fed 2 levels of S [low S (LS) vs. high S (HS)] at 2 forage-to-concentrate ratios (F:C). High S diet did not affect ruminal and blood thiamine status. Interestingly, however, HS diet showed increased brain thiamine levels. No gross or histopathological changes indicative of PEM were detected in the brains of the heifers. Of note, during the course of the present study, we documented an outbreak of S-induced PEM in commercial feedlot steers. Brain thiamine variables in experimental animals fed HS diet were then contrasted with brain thiamine status in PEM affected feedlot steers. Interestingly, in clinically normal animals, exposure to HS diet resulted in increased levels of both TMP and TPP in the brain tissue, in comparison to animals fed LS diet. In contrast, the PEM affected brains showed overall lower levels of thiamine phosphates. It is noteworthy that TPP levels were 36.5% lower, despite 4.9-fold higher free thiamine in PEM brains compared to normal brains. Our results indicate that high dietary S may increase the metabolic demand for TPP, and that animals incapable of maintaining requisite levels of brain TPP are at high risk to develop fulminant cerebrocortical necrosis.

The incidence of polioencephalomalacia and concentrations of ruminal hydrogen sulfide ([H 2 S]) in feedlot cattle appear to be greatest during the first 30 days of being fed a high sulfur (S) finishing diet. It was hypothesized that delaying exposure to high-S until cattle are fully adapted to a high-concentrate diet would reduce the peak [H 2 S], thus reducing potential for S-induced polioencephalomalacia. Sixty Angus crossbred-steers were moved into the feedlot and fed a moderate S (0.3% S) step-up diet for 7 days. Then steers were weighed (443±12.8 kg), blocked by weight, and randomly assigned to one of three dietary treatments: (1) two moderate-S (0.3% S) step-up diets fed for 7 d each (days 1–14) followed by a moderate S finishing diet (days 15–98; MS), (2) two high-S (0.6% S) step-up diets fed for 7 d each (days 1–14) followed by a high S finishing diet (days 15–98; HS), or (3) two moderate-S (0.3% S) step-up diets fed for 7 d each (days 1–14) followed by a moderate S finishing (0.3% S) diet for the first 28 days of the finishing period (days 15–42), followed by the high-S diet (0.6% S) for the remainder of the trial (days 43–98; Delayed S; DS). Ruminal [H 2 S] and pH were measured 6 h post-feeding on days 15, 21, 28, 42, 49, 56, 70, 84, and 98. The numerically greatest [H 2 S] (4948 mg/L) occurred in HS-steers on day 42 (28 d on the finishing ration) and on day 70 (28 d after starting high-S) for DS-steers (3690 mg/L). The maximum [H 2 S] of HS-steers tended to be greater ( P =0.09) than DS-steers, despite S intake not differing ( P =0.75). The elevated ruminal [H 2 S] of HS-steers on day 42, was likely not due to a decreased ruminal pH during adaptation to the finishing diet as pH did not differ due to treatment ( P =0.40) or day ( P =0.16). Overall, HS-steers had a 15% decrease (P=0.02) in average daily gain compared to MS-steers whereas gain of DS-steers was intermediate, not differing from MS ( P =0.13) or HS ( P =0.26) steers. These findings suggest that there may not be any additional increase in steer gains by delaying S inclusion in the diet until after the first 28 days of finishing, though it may decrease the maximum ruminal H 2 S concentration.

The rapid growth of the biofuels industry in the Midwest in the past 10 years has created an increased supply of corn coproduct feed for animals. This article discusses the tolerance and toxicology of biofuels coproducts in ruminants, including polioencephalomalacia, sulfur toxicosis, sulfur metabolism, mycotoxins, antibiotic residue, and biodiesel by-product toxicosis.

Literature describing nutritional or nutrition-related diseases of llamas and alpacas was reviewed. Case reports of copper toxicity, polioencephalomalacia, plant poisonings and urolithiasis accounted for the greatest number of literature citations relative to llamas and alpaca nutritional diseases. However, the overall number of published studies detailing nutritional disease of llamas and alpacas is very limited. Metabolic bone disease, associated with Vitamin D deficiency, and hepatic lipidosis were metabolic diseases for which controlled research studies were completed to address underlying mechanisms. Circumstantial evidence would suggest llamas and alpacas are similar to other ruminants relative to most nutrient deficiency or toxicity disease problems. Llamas and alpacas are unique compared to other ruminant animals in their susceptibility to zinc and Vitamin D deficiency diseases. A zinc-responsive dermatosis has been described, but the true role of zinc deficiency is debated. Llamas and alpacas show a seasonal deficiency in Vitamin D resulting in a hypophosphatemic rickets syndrome. Camelids may have a lower capacity to endogenously synthesize Vitamin D or higher requirement compared to other species. Although mechanisms are not fully understood, llamas and alpacas are somewhat different in metabolic responses to negative energy balance and subsequent hepatic lipidosis. Further research is necessary to better define llama and alpaca nutrient requirements and metabolism as they directly impact potential for nutritional disease. © 2005 Elsevier B.V. All rights reserved.

Polioencephalomalacia in general and the specific disorders associated with lead toxicosis and sodium imbalances all have commonalities in risk groups and clinical presentations but can be differentiated based on herd history, subtle clinical differences, and diagnostic tests. Treatment also has some overlap, but determining the specific etiology enables more specific treatment and more effective prophylactic measures.

Polioencephalomalacia (PEM) was induced in four of 10 lambs by the administration of a sulphide solution into the oesophagus at 20 min intervals for a period of 40 to 120 min. Signs of neurological dysfunction occurred in all 10 lambs during that time and included stupor, visual impairment and seizures. Gross autofluorescent and microscopic lesions in cerebrocortical grey matter were present as soon as 20 h after sulphide administration and were indistinguishable from lesions in naturally occurring disease. These findings, when considered together with an earlier study that revealed an association between high ruminal concentrations of sulphide and PEM, indicate that this disease can result from sulphide toxicosis, independent of the metabolic status of thiamine.

The effects of excess dietary sulphur were studied in sheep supplemented and unsupplemented with thiamine. The diets contained either 0.19 per cent sulphur (LS) or 0.63 per cent sulphur (HS) in combinations with 14 mg kg-1 thiamine (LB1) or 243 mg kg-1 thiamine (HB1). A total of 56 two-month-old lambs were used. Groups consisting of nine, nine, 22 and 16 lambs were fed LS-LB1, LS-HB1, HS-LB1 and HS-HB1 diets, respectively for 14 weeks. Out of 22 lambs fed the HS-LB1 diet, seven lambs developed neurological signs between the third and eighth week of the trial. Two of these lambs died, three that were in extremis were euthanased, and two recovered completely. All clinically affected animals had extensive malacic lesions in the cerebral cortex, midbrain and brainstem. None of the lambs from the LS groups or HS-HB1 group developed clinical signs. Several clinically normal lambs from the HS-LB1 group had necrotic lesions in their brains at gross and microscopic examination. Supplementation with dietary thiamine prevented development of clinical signs, but did not totally prevent development of microscopic brain lesions. Brain thiamine concentration, transketolase activity and thiamine pyrophosphate (TPP) effect were not different (P greater than 0.05) among groups. There was a strong effect (P less than 0.0001) of dietary thiamine supplementation on blood thiamine concentration and TPP effect. Blood thiamine concentration was higher whereas TPP effect was lower in the thiamine supplemented sheep. Blood and tissue thiamine concentrations in sheep exposed to high dietary sulphur did not indicate either systemic or local thiamine deficiency per se. Increased TPP effect in sheep fed the HS-LB1 diet indicated mild to moderate metabolic thiamine deficiency. Thiamine inadequacy may be an effect of an increased requirement for thiamine in animals exposed to excess dietary sulphur.

Analysis of cerebrospinal fluid (CSF) samples from normal sheep and from cases of some common neurological diseases revealed a significant increase (P less than 0.05) in the group mean CSF protein concentration for meningitis, listeriosis and spinal abscess but not for scrapie, spinal injury, ovine pregnancy toxaemia or polioencephalomalacia. The CSF white blood cell count (WBC) was significantly increased (P less than 0.05) in the meningitis group and in those cases of listeriosis which failed to respond to antibiotic therapy. All cases of bacterial infection of the central nervous system (CNS) could be identified by the combined interpretation of the protein concentration and the differential WBC count. It is concluded that CSF analysis is useful clinically in differentiating traumatic from infective spinal lesions and toxic or metabolic lesions from bacterial meningitis in sheep.

Three flocks in which one or more sheep had succumbed to polioencephalomalacia (cerebrocortical necrosis) were used for faecal thiaminase studies. Up to one third of the clinically normal animals in these flocks were found to be excreting thiaminase on any one day and over half the flock could be thiaminase excretors at some time during an outbreak. The possible detrimental effects of sub-clinical thiamine antagonism in sheep are therefore worthy of consideration. Thiaminase excretion by individual animals was variable and sometimes intermittent. It was unaffected by changes in diet, pasture or environment. In two of the flocks multiple cases of polio-encephalomalacia followed the administration of the anthelmintics, levamisole hydrochloride and thiabendazole. This aspect merits further investigation in view of the widespread use of anthelmintics of this type, especially as the profuse diarrhoea which can be associated with outbreaks of polioencephalomalacia may be wrongly attributed to gastro-intestinal parasitism.

Lesions of polioencephalomalacia (PEM, cerebrocortical necrosis) have been demonstrated in pre-ruminant lambs fed on synthetic, thiamine-free milk. Thiamine deficiency in these iambs was confirmed by transketolase assay.