Conceptual modeling of postmortem evaluation findings to describe dairy cow deaths.

Dairy cow mortality levels in the United States are excessive and increasing over time. To better define cause and effect and combat rising mortality, clearer definitions of the reasons that cows die need to be acquired through thorough necropsy-based postmortem evaluations. The current study focused on organizing information generated from postmortem evaluations into a monitoring system that is based on the fundamentals of conceptual modeling and that will potentially be translatable into on-farm relational databases. This observational study was conducted on 3 high-producing, commercial dairies in northern Colorado. Throughout the study period a thorough postmortem evaluation was performed by veterinarians on cows that died on each dairy. Postmortem data included necropsy findings, life-history features (e.g., birth date, lactation number, lactational and reproductive status), clinical history and treatments, and pertinent aspects of operational management that were subject to change and considered integral to the poor outcome. During this study, 174 postmortem evaluations were performed. Postmortem evaluation results were conceptually modeled to view each death within the context of the web of factors influencing the dairy and the cow. Categories were formulated describing mortality in terms of functional characteristics potentially amenable to easy performance evaluation, management oversight, and research. In total, 21 death categories with 7 category themes were created. Themes included specific disease processes with variable etiologies, failure of disease recognition or treatment, traumatic events, multifactorial failures linked to transition or negative energy balance issues, problems with feed management, miscellaneous events not amenable to prevention or treatment, and undetermined causes. Although postmortem evaluations provide the relevant information necessary for framing a cow's death, a restructuring of on-farm databases is needed to integrate this level of detail into useful monitoring systems. Individual operations can focus on combating mortality through the use of employee training related to postmortem evaluations, detailed forms for capturing necropsy particulars and other relevant information related to deaths, and standardized nomenclature and categorization schemes. As much as anything, the simple act of recognizing mortality as a problem might be the most fundamental step toward controlling its progression.

A necropsy-based descriptive study of dairy cow deaths on a Colorado dairy.

Increasing levels of dairy cow mortality pose a challenge to the US dairy industry. The industry's current understanding of dairy cow mortality is reliant upon descriptions largely based on producer or veterinary assumptions regarding cause of death without the benefit of detailed postmortem evaluations. A thorough necropsy is a superior tool for establishing a cause of death, except for cases involving euthanasia for traumatic accidents or severe locomotor disorders. Information provided from a necropsy examination would be most valuable if it were categorized and combined with cow health information in a complete postmortem evaluation designed to guide future management decisions. The objective of this study was to describe dairy cow deaths on a Colorado dairy over a 1-yr period and explore classification systems for necropsy findings that might inform management actions aimed at reducing dairy cow mortality. Throughout the study period a thorough necropsy examination was performed on every cow that died. Based upon this examination each death was characterized by a proximate cause (i.e., the most likely immediate cause of the death). Each proximate cause of death was then categorized using 3 alternate schemes founded on generalized etiologic principles and influenced by previous clinical history and treatments. These schemes included the broad categories commonly used for classifying findings within a review of literature related to dairy cow mortality, a diagnostic scheme used within the problem-oriented veterinary medical record, and an analysis focusing on the primary physiologic system derangement for each death. A total of 2,067 cows were enrolled during the study period of which 1,468 cows freshened, 507 cows were sold, and 94 cows died, resulting in a mortality risk of 6.4 deaths per 100 lactations at risk. The distribution of deaths by parity was significantly different from the herd distribution at the end of study with the largest percentage of death present in parity > or =4. Postmortem findings attributable to a specific cause of death were present for all but 4 of the 94 deaths. Assignment of the proximate causes of death to categories within the 3 alternate schemes provided a means for classifying necropsy findings and causes of death with different levels of detail. Creating categories with more selective groupings may provide a means for capturing specifics related to deaths that can be used to guide management decisions.

Association of severity of enteric granulomatous inflammation with disseminated Mycobacterium avium subspecies paratuberculosis infection and antemortem test results for paratuberculosis in dairy cows.

Disseminated infection (DI) of Mycobacterium avium subspecies paratuberculosis (MAP) in cattle may impair cow health, potentiate spread of disease, and is a potential food-safety risk. The objectives of this study were to determine the association between severity of histologic enteric lesions and the occurrence of DI, clinical signs, and positive fecal culture and serum ELISA results. Bacteriologic fecal culture and serum ELISA were performed on 40 dairy cows from MAP-infected herds. Cows were classified as having DI if MAP was isolated from any of 11 extra-intestinal tissues collected postmortem. A grade of 0-3, corresponding to the severity of histologically evident granulomatous inflammation was determined for sections of ileum, jejunum, mesenteric lymph node, and ileocolic lymph node. An overall intestinal inflammation (OII) grade of 0-3 was assigned to each cow. The proportion of cows with DI increased with tissue-specific lesion grade and OII grade. All cows with grade 3 inflammation in any single tissue had DI, however, some cows with DI had grade 1 inflammation or no lesions. In general, there was a positive association between OII grade and clinical signs, gross enteric lesions, and positive ELISA and fecal culture results. However, 12% of OII grade 0 cows had clinical signs (explained by other conditions recognized with necropsy), and the proportion of positive ELISA results was lower for OII grade 3 cows relative to grade 2 cows. Although MAP dissemination may occur early in the disease process, histopathology of intestinal tissues may be used to detect a substantial proportion of DI cows.

Pathology of radiation injury to the canine spinal cord.

The histopathologic response of the canine spinal cord to fractionated doses of radiation was investigated. Forty-two dogs received 0, 44, 52, 60, or 68 Gy in 4 Gy fractions to the thoracic spinal cord. Dogs were evaluated for neurologic signs and were observed for 1 or 2 years after irradiation. Six major lesion types were observed; five in the irradiated spinal cord and one in irradiated dorsal root ganglia. The three most severe spinal cord lesions were white matter necrosis, massive hemorrhage, and segmental parenchymal atrophy which had an ED50 of 56.9 Gy (51.3-63.3 Gy 95% CI) in 4 Gy fractions. These lesions were consistently associated with abnormal neurologic signs. Radiation damage to the vasculature was the most likely cause of these three lesions. The two less severe spinal cord lesions were focal fiber loss, which had an ED50 of 49.5 Gy (44.8-53.6 Gy 95% CI) in 4 gy fractions and scattered white matter vacuolation that occurred at all doses. These less severe lesions were not consistently associated with neurologic signs and indicated the presence of residual damage that may occur after lower doses of radiation. Radiation damage to glial cells, axons, and/or vasculature were possible causes of these lesions. In the irradiated dorsal root ganglia, affected sensory neurons contained large intracytoplasmic vacuoles, and there was loss of neurons and satellite cells. Such alterations could affect sensory function. The dog is a good model for spinal cord irradiation studies as tolerance doses for lesions causing clinical signs are close to the estimated tolerance doses for humans, and studies involving volume and long-term observation can be done.

Restoration of neutrophil and platelet function in feline Chediak-Higashi syndrome by bone marrow transplantation.

Allogeneic bone marrow transplantation (BMT) was successfully performed in four Chediak-Higashi (CHS) syndrome affected cats. Preparatory regimens included selective intestinal flora decontamination, fractionated total body irradiation for myeloablation, and prophylactic treatment for graft-versus-host disease with cyclosporin A. Neutrophil chemotaxis under-agarose and whole-blood platelet aggregation/secretion were characterized prior to BMT and after engraftment of donor-origin marrow cells. Liver and kidney biopsies were obtained and evaluated by light and electron microscopy before, and at 6 months post-BMT to determine what effect BMT might have on abnormal lysosome fusion in hepatocytes and renal tubule cells. The platelet storage pool defect was resolved by day 40 post-BMT. In vitro neutrophil migration in all cats appeared to improve with time after BMT and complete restoration was evident by day 175 post-BMT. No apparent differences were evident in either the liver or the kidney at 6 months post-BMT. One cat developed seizures and one developed posterior paresis 5 months post-BMT; neurologic impairment ultimately resulted in death of two cats at 6 and 8 months post-BMT, respectively. Neurologic lesions in both cats were characterized by non-suppurative encephalitis. Allogeneic BMT successfully corrected the neutrophil migration defect and platelet storage pool deficiency but had no effect on lysosome distribution in liver and kidney cells of CHS cats.

Brain enzyme and clinical alterations induced in rats and mice by nitroaliphatic toxicants.

The effects of a single subcutaneous (s.c.) injection of the nitroaliphatic toxicants 3-nitropropanol (NPOH) and 3-nitropropionic acid (NPA) dissolved in physiological saline solution were studied in mice and rats, respectively. Clinical signs observed in both NPOH-treated mice and NPA-treated rats included depression, abnormal motor activity, and recumbency. Succinate dehydrogenase (SDH) activity, demonstrated histochemically in frozen brain sections, was markedly reduced in intoxicated mice and rats. The SDH activity of mitochondrial preparations from brains of intoxicated mice and rats was diminished to 18-24% of control values, although the activity of another mitochondrial flavoprotein enzyme, alpha-glycerophosphate dehydrogenase (alpha-GPDH), was not altered.

Mutagenicity tests of diflubenzuron in the micronucleus test in mice, the L5178Y mouse lymphoma forward mutation assay, and the Ames Salmonella reverse mutation test.

Diflubenzuron, one of a new class of pesticides believed to act via inhibition of chitin synthesis in the developing insect cuticle, was tested for possible mutagenic activity using the micronucleus test in mice, the L5178Y mouse lymphoma forward mutation test at the thymidine kinase locus, and the Ames Salmonella/microsome reverse mutation test. No mutagenic effect was found.

The effect of glutathione depletion by buthionine sulphoximine on 1-cyano-3,4-epithiobutane toxicity.

The effect of glutathione (GSH) depletion by buthionine sulphoximine (BSO) on the nephrotoxicity and GSH-enhancing effect of the naturally occurring, crucifer-derived nitrile 1-cyano-3.4-epithiobutane (CEB), was investigated. Male Fischer 344 rats were administered 50 or 125 mg CEB/kg body weight by gavage with or without prior ip treatment with 550 mg/kg body weight L-BSO. One group of control animals was treated with water only by gavage, while another group was pretreated with BSO and then given water by gavage. Liver and kidney samples were taken 48 hr after CEB treatment for GSH determinations and histological examination. The high-dose CEB without BSO resulted in increased GSH in liver and kidney, marked karyomegaly in the pars recta of renal proximal tubules and tubular epithelial necrosis, which was limited to a few renal tubules. The low-dose CEB alone resulted in increased hepatic GSH and mild karyomegaly. Pretreatment with BSO abrogated the tubular necrosis and karyomegaly induced by either CEB dose. BSO pretreatment inhibited low-dose CEB-induced GSH enhancement in the liver. The combined BSO and high-dose CEB treatment still resulted in increased hepatic GSH, although the increase was less than that observed with high-dose CEB alone. In the kidney, BSO pretreatment abrogated the high-dose CEB-induced increase in GSH, but GSH content was not significantly different from that with high- or low-dose CEB alone. These results provide evidence that CEB conjugation may be a bioactivation reaction with the conjugate involved in nephrotoxicity. The conjugate may also be involved in increasing renal and hepatic GSH.

Selective pancreato-toxicity in the rat induced by the naturally occurring plant nitrile 1-cyano-2-hydroxy-3-butene.

The acute toxicity of 1-cyano-2-hydroxy-3-butene (CHB), a nitrile derived from many cruciferous plants, was investigated. Young male CDF (F-344/CrlBr) rats were treated by gavage once daily with 200 mg (2.1 mmol) CHB/kg body weight for 0-4 days and killed 24 hr after the final dose. Lesions were confined to the exocrine pancreas and characterized by individual acinar cell death, inflammation and acinar atrophy and disorganization. Ultrastructural alterations included dilation of cisternae of the acinar cell endoplasmic reticulum, acinar cell death resembling apoptosis, macrophage phagocytosis of acinar cell debris and regenerative changes in remaining acinar cells. Pancreatic, hepatic and renal non-protein thiol concentrations were elevated, suggesting an enhancement of tissue glutathione concentrations and an alteration in glutathione metabolism. Urinary thiocyanate (SCN-) excretion was modestly elevated, indicating some in vivo cyanide release from this nitrile. The results of this study indicate that CHB is a selective pancreatotoxin, inducing changes consistent with apoptosis. CHB is also a possible inducer of tissue glutathione in the liver and kidneys as well as in the pancreas, even at toxic doses.

Sequential changes in hepatic and renal glutathione and development of renal karyomegaly in 1-cyano-3,4-epithiobutane toxicity in rats.

The effect of 1-cyano-3,4-epithiobutane (CEB) on glutathione (GSH) metabolism was investigated in rat liver, kidney and pancreas. Male Fischer 344 rats were gavaged with a single dose (125 mg/kg body weight or 50 mg/kg body weight) of CEB. Tissue samples were taken for histological examination, determination of GSH and oxidized glutathione (GSSG) concentrations and gamma-glutamyl transpeptidase (GGT) and glutathione S-transferase (GST) activities. Urine samples were analysed for non-protein thiol (NP-RSH) content. The high dose of CEB induced hepatic GSH depletion followed by increased GSH. The low dose of CEB induced elevated hepatic GSH by 12 hr without depletion. Renal GSH was increased with both doses without an observed depletion phase. Renal tubule epithelial cell death was observed only with the high dose of CEB, but both doses caused renal proximal tubule karyomegaly. Pancreatic GSH content was unaffected. No alterations of GSSG were observed. GST activity was unaffected in any tissue. Renal GGT activity was decreased at 12 hr with both doses and at 24 and 48 hr with the high dose. Urinary NP-RSH excretion was increased with both doses. Depletion of hepatic GSH concurrent with increased urinary NP-RSH excretion suggests that conjugation with GSH is a significant pathway in CEB metabolism.

Comparative toxicities of the naturally occurring nitrile 1-cyano-3,4-epithiobutane and the synthetic nitrile n-valeronitrile in rats: differences in target organs, metabolism and toxic mechanisms.

Toxic but sublethal oral doses of 125 mg/kg (1.1 mmol/kg) of the cruciferous nitrile, 1-cyano-3,4-epithiobutane (CEB), or 175 mg/kg (2.1 mmol/kg) of its synthetic saturated analogue, n-valeronitrile (VN), were given by gavage to male CDF (F-344/CrlBr) rats once daily for 1, 2 or 3 days, in order to compare target tissues and to observe structure-activity relationships between the nitriles. CEB-induced changes included degeneration and necrosis of the pars recta of the renal proximal tubules, ulceration and necrosis in the forestomach, a mild increase (4.5-fold) in daily urinary thiocyanate (SCN-) excretion (only in rats treated for 3 days) and 1.5- to 2.4-fold increases in hepatic and pancreatic non-protein thiol (RSH) concentrations (in all CEB-treated groups). In VN-treated rats, there were no consistent histological changes but 95- to 170-fold increases in daily urinary SCN- excretion, delayed clinical signs of cyanide toxicity and minimal effects on tissue RSH concentrations. These results indicate different toxic mechanisms for VN and CEB. The nephrotoxic effects of CEB were very similar to those of 1-cyano-2-hydroxy-3,4-epithiobutane, suggesting a role for the epithio group in the nephrotoxicity of these nitriles. The relatively low SCN- excretion in CEB-treated rats also suggested that cyanide played only a minimal role in CEB toxicity, while the high SCN- excretion, clinical signs of cyanide poisoning and lack of histological changes imply a greater role for metabolically-derived cyanide in VN toxicity. The enhancement of tissue RSH by CEB treatment with indications of enhanced tissue glutathione concentrations suggested the involvement of glutathione in the detoxication of CEB and/or its reactive metabolites.

Potential for disruption of central nervous system tissue in beef cattle by different types of captive bolt stunners.

The application of pneumatic-powered air injection stunners (PPAISs), pneumatic-powered stunners (PPSs), and cartridge-fired stunners (CFSs) in commercial beef slaughter plants was evaluated to determine the extent of dissemination of central nervous system tissue. Fifteen beef slaughter plants in the western and central United States were visited to observe stunning methods and the condition of the hearts at postmortem inspection. As inspectors performed the normal opening of the hearts, the research observer evaluated the contents of the heart for the presence of clots and/or visible tissue segments in the right ventricle. In eight plants where PPAISs were used, 33% of hearts examined (n = 1,050) contained large clots in the right ventricles. In the four plants where CFSs were used, 1% of the hearts (n = 480) contained detectable clots. In three plants where the newly modified PPSs were used, 12% of the hearts (n = 450) contained detectable clots. Large segments of spinal cord were detected, collected, photographed, and confirmed histologically from two hearts in a plant that used a PPAIS. Most of the material was found in a single right ventricle and was composed of 10 to 13 cm segments of spinal cord.

An enzyme-linked immunosorbent assay for glial fibrillary acidic protein as an indicator of the presence of brain or spinal cord in meat.

The current methods to detect central nervous system (CNS) tissue in blood, lungs, or meat are cumbersome, time consuming, and costly. The objective of this study was to use glial fibrillary acidic protein (GFAP), which is restricted to the CNS, in an enzyme-linked immunosorbent assay (ELISA) for the detection of CNS tissue in blood and muscle from beef cattle. Bovine brain, cerebral cortex, spinal cord, sciatic nerve, diaphragm, blood clots, and other skeletal muscle were obtained from three animals at slaughter. The limit for detection of GFAP was approximately 1.0 ng and the standard curve was linear up to 40 ng. Tissue samples gave responses parallel to the GFAP standard, suggesting that standard and unknown samples were immunoreactively identical. No GFAP was detected in skeletal muscle (ground beef, shoulder clod, and diaphragm) and blood clots. Trace amounts (13.5 to 51 ng/mg) were present in sciatic nerve. In contrast, high levels of GFAP (55 to 220 microg/ mg) were present in spinal cord, cerebral cortex (17 microg/mg), and whole brain (9 to 55 microg/mg). In a storage study using two animals in two separate studies, immunoreactive GFAP was detectable for up to 8 days at 4 degrees C in all tissues containing neural elements. Thus, mixtures of muscle with spinal cord or brain retained almost 80% of their immunoreactivity after 8 days at 4 degrees C, while brain and spinal cord alone retained approximately 50% and 25%, respectively, of their initial activities. In a repeat experiment, 80 to 100% of the initial activity was retained in these tissues after 8 days at 4 degrees C. The results of the current study demonstrate that the GFAP ELISA provides a valid and repeatable method to detect CNS tissue contamination in meat.

In vivo indicators of pathologic ruminal sulfide production in steers with diet-induced polioencephalomalacia.

Two groups of 3 120-160-kg Holstein steers were fed a diet high in carbohydrate and low in long fiber and either with or without added sodium sulfate. Prior to and during the course of feeding the experimental diet, the concentrations of rumen hydrogen sulfide gas and rumen fluid sulfide were determined by a simple sulfide detector tube method and by sulfide-selective electrode, respectively. Other measurements included rumen fluid pH, blood creatine kinase, and blood sulfhemoglobin. Two of the 3 steers fed the high-sulfate diet developed signs and lesions of polioencephalomalacia. Clinical signs included episodic ataxia and blunted or absent menace reaction. Increased ruminal H2S gas concentrations occurred in all 3 steers consuming the diet with added sulfate. The onset of clinical signs coincided with the onset of elevated H2S concentrations. These increases were 40-60 times the values measured in the steers consuming the diet without added sulfate. In contrast, increases in rumen fluid sulfide concentrations usually rose to 4 times that of control steers. The steers fed an identical diet but without added sulfate exhibited no signs or lesions of polioencephalomalacia and no elevations of sulfide in rumen gas or fluid. All steers had a modest decrease in rumen fluid pH associated with the transition to the concentrate diet. No significant changes were observed in any of the blood measurements of any of the steers. An additional pair of steers was fed the experimental diet with or without added sulfate to compare the ruminal H2S gas concentrations estimated by H2S detector tubes with those estimated by a different method of analysis utilizing charcoal trapping of H2S, conversion to sulfate, and measurement of the sulfate. Both methods yielded comparable estimates of H2S concentration. Overall, these data indicate that changes in rumen gas cap H2S concentrations are larger than changes in rumen fluid sulfide concentration and the estimation of rumen gas cap H2S concentration may be a practical approach to detecting pathologic increases in ruminal H2S gas. This simple, rapid, minimally invasive method should be useful for estimating the H2S content of ruminal gas under field conditions.

Biological effects of alkali-treated protein and lysinoalanine: an overview.

The renal alterations induced by alkali-treated protein and lysinoalanine are reviewed and their biological implications discussed. Alkali-treated proteins and lysinoalanine, an unusual amino acid formed in proteins during alkali treatment, have been shown to produce a renal alteration characterized by nuclear and cytoplasmic enlargement, with alterations in DNA synthesis, mitotsis and nucleoprotein. These changes are localized in the straight portion of the proximal renal tubule and have been observed in rats but not in several other species. The nephrotoxic effect of synthetic lysinoalanine has been consistently demonstrated, but the ability of alkali-treated protein to induce renal alterations is apparently modified by factors other than lysinoalanine content. Factors which may influence the development of the kidney lesions in animals fed alkali-treatment protein are discussed, including nutritional factors, the chemical form of lysinoalanine in the protein, species differences, and metabolic fate. Other clinical and experimental conditions that result in similar renal alterations are presented for comparison with the lysinoalanine induced lesion, and possible functional consequences are considred.

Sulphide-induced polioencephalomalacia in lambs.

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.

Polioencephalomalacia.

Polioencephalomalacia (PEM) is a neuropathologic condition of ruminants that can be induced by a variety of neural metabolic disruptions. These include altered thiamine status, water deprivation-sodium ion toxicosis, lead poisoning, and high sulfur intake. Investigations of sulfur-related PEM have demonstrated that the onset of the clinical signs coincides with excessive ruminal sulfide production. A number of ruminal factors could modulate the production and absorption of ruminal sulfide. The development of a convenient method to estimate ruminal gas cap H2S has made it possible to identify cattle with high levels of ruminal H2S and evaluate their risk of developing PEM.

Effects of water sulfate concentration on performance, water intake, and carcass characteristics of feedlot steers.

Two hundred forty single-source, cross-bred steers (304 kg) were used to evaluate the effects of various water sulfate concentrations on performance, water intake, and carcass characteristics of feedlot steers. Cattle were stratified by weight and assigned within weight blocks to five water treatments. Averaged over time, actual water sulfate concentrations (+/- SEM) were 136.1 (+/- 6.3), 291.2 (+/- 15.3), 582.6 (+/- 16.9), 1,219.2 (+/- 23.7), and 2,360.4 (+/- 68.2) mg/L, respectively. Weather-related data were recorded. Increasing water sulfate concentration resulted in linear decreases in ADG (P < 0.01) and gain:feed ratio (P < 0.01) and a quadratic effect on water intake (P = 0.02) and tended to quadratically increase then decrease DMI (P = 0.13). Sulfate x period interactions were evident for DMI (P = 0.01), ADG (P < 0.01), and feed efficiency (P < 0.01). Time had quadratic effects on DMI, water intake, ADG, and feed efficiency (P < 0.01 for all models). Increasing water sulfate concentration resulted in linear decreases in final weight, hot carcass weight, and dressing percentage, a linear increase in longissimus muscle area, and a quadratic effect on fat thickness over the 12th rib and predicted yield grade (P < 0.05 for all dependent variables). Mean daily temperature explained 25.7% of the observed variation in water intake. Other factors that explained a significant (P < 0.01) amount of variation in water intake were BW, DMI, water sulfate concentration, barometric pressure, wind speed, and humidity. High water sulfate concentrations had a significant and deleterious effect on performance and carcass characteristics of feedlot steers. Increasing the sulfate concentration in water may have resulted in a functional water restriction early in the trial when ambient temperatures were greatest. However, toward the latter stages of the trial, cattle supplied higher-sulfate water had higher ADG and FE. These improvements later in the trial may represent compensatory gain associated with decreased ambient temperature and water requirements. Averaged over time, a water sulfate concentration of greater than 583 mg/L, equivalent to 0.22% of the diet, decreased feedlot performance.

Clinical and biochemical alterations in calves with nutritionally induced polioencephalomalacia.

Polioencephalomalacia (PEM) was induced in calves by feeding a semipurified, low-roughage diet of variable copper and molybdenum composition. Two formulations resulting in Cu-insufficient and Cu-sufficient forms of the diet were fed (n = 10 and 4 calves, respectively); both diets induced PEM. Clinical signs of disease developed as early as 15 days after transition to the experimental diets and included impaired vision, decreased response to external stimuli, and abnormal gait. Grossly evident cerebrocortical lesions consisted of laminar areas of cavitation and/or autofluorescence seen under UV illumination. Hepatic Cu concentration was decreased in calves fed the Cu-insufficient diet, but not below normal range. During the course of feeding either diet, rumen pH decreased, rumen volatile fatty acid concentrations increased, rumen and blood lactic acid concentrations increased, and rumen and plasma thiamine concentrations increased. The thiamine pyrophosphate effect on erythrocyte transketolase activity was unaltered in calves of either diet group. This nutritionally induced form of PEM does not appear to be related to Cu deficiency or reduction in plasma or rumen thiamine concentration.

High sulfide concentrations in rumen fluid associated with nutritionally induced polioencephalomalacia in calves.

Nine 115- to 180-kg, hay-adapted, Holstein steers were fed an experimental diet with added sodium sulfate that induces polioencephalomalacia (PEM). Five calves developed the disease. Thiamine concentrations in blood, CSF, brain, and liver were not indicative of thiamine deficiency. The odor of hydrogen sulfide in eructated rumen gas was associated with the onset of PEM. Sulfide concentrations in rumen fluid were measured 1 or 2 times a week by 2 techniques. Sulfide concentrations progressively increased in all 9 calves after the feeding of the PEM-inducing diet commenced. The highest concentrations coincided with the onset of clinical signs of PEM and were significantly higher in the calves that developed PEM than in those that did not. This suggests that PEM can result from sulfide toxicosis following excess production of sulfide in the rumen.