Ovine white-liver disease (OWLD). Changes in blood chemistry

Changes in blood chemistry were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), and were compared with values of cobalt/B12 supplemented lambs on the same pastures, as well as clinically healthy, but sometimes B12 deficient, lambs on other pastures (H). In the OWLD group, signs of hepatic damage were seen concurrently with reduction in weight gain, or 1-3 weeks before, and comprised elevation of serum glutamate dehydrogenase (GLDH) and decrease of phospholipid and cholesterol. Drop of plasma glucose and elevation of gamma GT also came in the earlier phase of the disease. All other blood changes developed later, and were partly regarded as reflections of the inappetence or hepatic injury. The changes included a drop in packed cell volume (PCV) and mean corpuscular volume (MCV), elevation of serum iron, and reduction of total serum protein and urea. Generally Co/B12 supplementation prevented hepatic damage and normalized blood values. The clinically healthy H lambs also showed signs of hepatic damage, especially one year when they were B12 deficient, indicating that simple B12 deficiency causes a moderate liver damage as well. For diagnostic purposes, clinical pathology is recommended mainly on a flock basis.     

Ovine white-liver disease (OWLD). Trace elements in liver

Trace elements in liver were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), in cobalt/vitamin B12 supplemented lambs on the same pastures as well as clinically healthy, but sometimes subclinical B12 deficient lambs on other pastures (H). Liver Co was marginal to deficient in both OWLD lambs (S lambs) and H lambs. Supplementation with B12 or Co elevated liver Co. Liver copper was significantly lower in OWLD lambs than in the H lambs, and Co/B12 supplementation on pasture generally had no significant effect on the contents. Dosing lambs on OWLD pastures with copper oxide needles (SCuO), however, resulted in high/toxic liver Cu. Dosing with Co, Se and Cu glass boluses resulted in adequate liver Cu, except for 1 lamb with toxic amounts indicating dissolution and absorption of the bolus. OWLD lambs had significantly lower liver molybdenum than H lambs, and Co/B12 supplementation elevated values, while CuO treatment depressed them. Liver zinc, manganese and selenium are also reported.     

Ovine white-liver disease (OWLD) in Norway: clinical symptoms and preventive measures

During 6 years, altogether 458 twin lambs of the Dala and Rygia breeds with their dams were put on ovine white-liver disease (OWLD) pastures which were moderately, heavily or not cobalt fertilized, or on control pastures 15 km apart. Groups of lambs were untreated, regularly dosed with Co sulphate or vitamin B12, dosed with Co pellets, copper oxide needles (CuO), selenium pellets or Co-Se-Cu glass boli, or had access to Co enriched salt lick. Clinical symptoms in untreated lambs included varying degree of reduced weight gain or loss of weight appearing after 6-12 weeks on pasture, at an age of 10-15 weeks. Additional symptoms were seen 2-4 weeks later, including inappetence, listlessness, and often serous eye discharge and crusty ears. Of the untreated lambs on OWLD pastures 18% died or were eutanized because of OWLD. The condition was preventable by Co or B12 administration, which yielded an average increase of mid Sept. live weights of between 8 and 17 kg. Co fertilization of pastures, use of Co enriched salt lick, or dosing with Co pellets are recommended under practical circumstances. The lambs grazing control pastures were on average 17 kg heavier by mid Sept. than the OWLD lambs. They showed some weight increase on extra Co supply.     

Ovine white-liver disease (OWLD). Serum copper and effects of copper and selenium supplementation

Serum copper was generally higher in lambs affected with ovine white-liver disease (OWLD) than in cobalt/vitamin B12 supplemented lambs grazing the same pastures. Although the copper content of the grass was very low on the OWLD pastures, dosing lambs with Cu alone resulted in worsening of the clinical condition and aggravation of clinical pathology. Dosing with selenium had no effect on OWLD. Dosing with a combination of Co, Se and Cu resulted in normal lamb growth and normal laboratory tests. Lambs growing well on other pastures (H) showed elevated serum Cu when they were subclinically B12 deficient.     

Ovine white-liver disease (OWLD). Vitamin B12 and methyl malonic acid (MMA) estimations in blood

At pasture outlet, mean plasma vitamin B12 varied between 210 and 1,200 pmol/l in 1 month old lambs, 19% of them had values below 250 pmol/l. In those put on OWLD pastures, mean values dropped after 2-4 weeks, and mostly stayed below 150 pmol/l throughout grazing. Plasma methylmalonic acid (MMA) rose above 5 mumol/l 2-8 weeks after outlet, and above 15 mumol/l 4 weeks later. Reduced growth occurred 3-8 weeks after plasma B12 dropped below 150 pmol/l, and 4-6 weeks after MMA rose above 5 mumol/l. Clinical OWLD was most often associated with plasma B12 less than 150 pmol/l and MMA greater than 15 mumol/l. Cobalt fertilization of pastures induced satisfactory plasma B12/MMA values for 3 succeeding years. Elevated plasma B12 was found 3 weeks after Co pellet dosing. The use of Co lick resulted in large individual variations in plasma B12/MMA. The control lambs, which were healthy and grew well on pastures which some years contained marginal/deficient cobalt, had plasma B12/MMA values which varied considerably. One year values indicated functional Co deficiency, but none developed OWLD, and growth was satisfactory, but less than other years. In these lambs, high MMA was not always associated with low B12, or depressed growth. OWLD occurred in Co/B12 deficient lambs, but Co/B12 deficient lambs on other pastures did not develop OWLD.     

Ovine white-liver disease (OWLD). Botanical and chemical composition of pasture grass

The most important grass species on the ovine white-liver disease (OWLD) pastures (S) were Poa spp., Agropyron repens and Lolium perenne, while the control pastures (H), where lambs grew well, consisted of Poa spp., Festuca rubra and Agrostis tenuis. The soil was more acidic on the H pastures as compared with the S pastures. OWLD grass (S grass) contained marginal to deficient amounts of cobalt during the first 2 months of grazing. During 2 years out of 3, the average Co content was slightly lower in the S grass as compared with the content in the H grass. The lowest average grass Co was, however, found during one year in the H grass, in spite of the fact that the H lambs also this year grew well, and were 13 kg heavier than the S lambs after 3 1/2 months on pasture. Results thus indicate that the H lambs some years were subclinically Co deficient, without developing clinical symptoms or OWLD, and that factors other than marginal/deficient grass Co are of importance as to whether OWLD will develop or not. S grass differed from H grass by having significantly lower copper, molybdenum, manganese and zinc content, lower protein N/amid N ratios and higher aluminium and iron contents. According to the results, marginal to deficient grass Co is essential for development of OWLD, but cofactors play a part.     

Glycogen accumulation and histological changes in the livers of lambs with alveld and experimental sporidesmin intoxication

Alveld is a hepatogenous photosensitization disease seen in lambs grazing Narthecium ossifragum pastures in Norway. Mycotoxins, possibly sporidesmin, have been suspected to cause the liver damage in alveld as in facial eczema. The histological changes in the liver of alveld cases and in lambs photosensitized after experimental sporidesmin intoxication were compared. The liver damage characterized by necrosis in single centrilobular hepatocytes, was of the same type in both conditions. Minor to moderate portal fibroplasia and bile duct proliferation were almost always present. Accumulated glycogen was seen in hepatocytes in the centrilobular areas. This was significantly correlated to the enzymatically measured glycogen content and there was good correlation between parenchymal damage and glycogen accumulation. The glucose-6-phosphatase and glycogen phosphorylase activities were normal. These findings indicate that parenchymal damage, rather than obstruction of the bile ducts, caused the retention of phylloerythrin both in alveld cases and in experimentally sporidesmin-intoxicated lambs. The accumulation of glycogen could not be explained.Abbreviations HE haematoxylin and eoson - PAS periodic acid Schiff - EDTA ethylene diamine tetracetic acid     

Pathological changes in cobalt-supplemented and non-supplemented twin lambs in relation to blood concentrations of methylmalonic acid and homocysteine.

In a controlled field study of three years' duration we evaluated the effect of cobalt supplementation on pathological changes in cobalt/vitamin B12-deficient Texel twin lambs grazing the same cobalt-deficient pasture. Semi-quantitative evaluation of the histopathology of liver and brain was done on 44 sets of twins. Pathological changes were related to blood concentrations of vitamin B12, methylmalonic acid, and homocysteine. Lesions were mainly confined to the liver and brain. Acute hepatic changes were characterized by steatosis, hepatocytic degeneration, and single cell necrosis. Chronic changes consisted of bile duct proliferation, the presence of ceroid containing macrophages, and fibrosis in the portal triads. Many non-supplemented lambs showed polymicrocavitation and Alzheimer type II reaction in the brain. Polioencephalomalacia was observed in three non-supplemented lambs but was regarded as a secondary lesion. Our results indicate that the main lesions found in cobalt/vitamin B12-deficient lambs are acute and chronic hepatitis. These lesions were associated with low concentrations of vitamin B12 and high concentrations of methylmalonic acid and homocysteine in the blood. The liver lesions were also associated with polymicrocavitation of the brain, probably as morphological evidence of hepatoencephalopathy.     

The effect of increasing the Vitamin B12 status of Romney ewes on foetal liver Vitamin B12, milk Vitamin B12 and liver Vitamin B12 concentrations in suckling lambs

AIM: To determine the effect of increasing the Vitamin B12 status of the ewe on the Vitamin B12 supply to the suckling lamb. METHODS: The Vitamin B12 status of the ewe was increased during gestation and lactation by three injections of a long-acting preparation of Vitamin B12 microencapsulated in an organic acid polymer. The Vitamin B12 status of the ewes and suckling lambs was assessed from changes in serum and liver Vitamin B12 concentrations. RESULTS: Compared to untreated animals, serum and liver Vitamin B12 concentrations of the treated ewes were increased at least 70% during gestation. Foetal liver Vitamin B12 concentrations were increased 270%. Over the lactation, ewe serum and milk Vitamin B12 concentrations were increased at least 200% and 44%, respectively. The liver Vitamin B12 stores of the newborn lambs from Vitamin B12-treated ewes were depleted within 58 days. There were no significant differences in the serum Vitamin B12 concentrations of suckling lambs from Vitamin B12-treated and untreated ewes. CONCLUSION: Ewes with a high Vitamin B12 status will ensure an adequate supply of Vitamin B12 to their lambs for at least the first 30 days of life. CLINICAL SIGNIFICANCE: In flocks grazing Co-deficient pastures, treating ewes with a long-acting Vitamin B12 supplement at mating will prevent Vitamin B12 (Co) deficiency in ewes, as well as their lambs, until they can be treated at tailing at 4-6 weeks of age.     

Accumulation of Sapogenin Conjugates and Histological Changes in the Liver and Kidneys of Lambs Suffering from Alveld,a Hepatogenous Photosensitization Disease of Sheep Grazing Narthecium ossifragum

Sixteen lambs exhibiting hepatogenous photosensitization (alveld) after grazing pasture containing Narthecium ossifragum and seven nonphotosensitized lambs grazing the same pastures were studied. All the alveld-affected lambs revealed liver damage dominated by single cell necrosis, portal fibroplasia and bile duct proliferation. Crystalloid clefts were demonstrated in the bile ducts of two and in the hepatocytes and Kupffer cells of nine photosensitized lambs. Plasma bilirubin concentration was severely increased in ten of the cases of alveld whereas the activity of aspartate aminotransferase was moderately to severely increased in seven cases. The activity of glutamate dehydrogenase was moderately elevated in one of the photosensitized lambs. The main histopathological findings in the kidneys from the alveld-affected lambs were dilated tubules, often with eosinophilic material in the tubular lumina. Regenerative changes were seen in a large proportion of the renal sections. Elevated plasma concentrations of urea and creatinine, and the renal histopathological changes, suggested that the photosensitized lambs had been through a phase of renal injury. Analysis of the free and conjugated sapogenin content in liver tissue and bile was performed by gas chromatography–mass spectrometry. There were significantly higher concentrations of conjugated episapogenins in both the liver and bile in the alveld-affected lambs than in the nonphotosensitized lambs.     

Growth response to increasing doses of microencapsulated vitamin B12 and related changes in tissue vitamin B12 concentrations in cobalt-deficient lambs

AIM: To investigate growth response of cobalt deficient lambs to increasing doses of microencapsulated vitamin B12, and to measure associated changes in serum and liver vitamin B12 concentrations over 243 days. METHODS: From a flock grazing pastures that had low cobalt (Co) levels (about 0.06 mg Co/kg dry matter), 4-6-week-old lambs (n=137) were assigned to four groups and received either no treatment or a subcutaneous injection of 3.0, 4.5 or 6.0 mg of microencapsulated vitamin B12 on Day 1. At approximately monthly intervals, all lambs were weighed and blood samples were collected from a selection (n=10) of monitor animals, up to Day 243. Liver biopsies were also carried out on the monitor lambs (n=8) on Days 1, 124 and 215. RESULTS: The vitamin B12-treated lambs grew significantly faster (p<0.001) than untreated animals. Liveweights after 243 days were 28, 45, 45 and 47 kg for the untreated, 3.0, 4.5 and 6.0 mg vitamin B12-treated lambs, respectively. Of the initial group of untreated lambs, 68% had to be removed before the end of the trial because of substantial weight loss, but none of the treated animals were similarly afflicted. Serum vitamin B12 concentrations increased in all vitamin B12-treated lambs, reaching a peak at Day 25, and those of the 4.5 and 6.0 mg vitamin B12-treated lambs remained significantly higher (except at Day 124) than the untreated lambs to Day 187. However, at Day 124, but not Day 215, the liver vitamin B12 concentrations of treated lambs were two to three times higher than those of controls. CONCLUSIONS: The growth rates of Co deficient lambs were markedly improved by injection of 3.0, 4.5 or 6.0 mg of microencapsulated vitamin B12, and liveweights were maintained for at least 243 days. Serum vitamin B12 concentrations were related to this growth response; concentrations of <220 pmol vitamin B12/l were associated with a 95% probability that lambs were Co deficient and would thus respond to Co/vitamin B12 supplementation. Based on these data, the current New Zealand reference criteria for Co deficiency should be reviewed. CLINICAL SIGNIFICANCE: An injection of 3 mg microencapsulated vitamin B12 given to lambs at tailing will treat Co deficiency and will increase and maintain liveweights in a flock for up to 8 months.     

The pathology of experimental Lasiospermum bipinnatum (Thunb.) Druce (Asteraceae) poisoning in sheep. I. Hepatic lesions

Poisoning with the plant Lasiospermum bipinnatum was studied in 9 lambs. Intraruminal doses, varying from 1-12 g/kg/day of dried plant, were administered to 8 animals and 1 was fed 2.5 g/kg/day of the material mixed with maize meal for 13 days. Periodic serum analyses were done to monitor liver function. Lambs given 6-12 g/kg/day died or were killed in extremis. Clinical signs included progressive anorexia and depression in all these lambs and icterus in 2 animals. Lambs given 1-4 g/kg/day were sacrificed after about 2 weeks. Clinical signs in these animals were minimal or absent. Hepatosis was found in all the lambs, the severity of which correlated with levels of plant administered. Centrilobular necrosis and haemorrhage occurred in 2 of the 4 lambs given high doses; single cell necrosis of hepatocytes was observed with intermediate doses, and diffuse degeneration, which was more severe peripherally, was seen at various doses. In 1 lamb, degeneration was most severe midzonally. Bile ductule epithelial proliferation was observed in 7 of the 9 poisoned animals. Marked hypertrophy of hepatocellular smooth endoplasmic reticulum was seen in 3 lambs given low doses. The hepatic lesions were compared with those reported for poisoning by other hepatotoxic plants belonging to the family Asteraceae and found to be indistinguishable.     

Dose response effects of long-acting injectable vitamin B12 plus selenium (Se) on the vitamin B12 and Se status of ewes and their lambs

AIM: To determine the effect of increasing doses of long-acting injectable vitamin B12 plus selenium (Se) given pre-mating on the vitamin B12 and Se status of ewes and their lambs from birth to weaning. METHODS: Four groups of 24 Poll Dorset ewes each were injected 4 weeks pre-mating with different doses of a long-acting vitamin B12 + Se product, containing 3 mg vitamin B12 and 12 mg Se per ml. The treatment groups received 5 ml (15 mg vitamin B12 + 60 mg Se), 4 ml (12 mg vitamin B12 + 48 mg Se), 3 ml (9 mg vitamin B12 + 36 mg Se), or no vitamin B12 or Se (control). Twelve of the twin-bearing ewes per group were selected for the study. Efficacy of the product was evaluated from changes in the concentrations of vitamin B12 in serum and liver, and of Se in blood, liver and milk in the ewes during gestation and lactation, and in their lambs from birth to weaning. Pasture samples in paddocks grazed by the ewes and lambs were collected at about 2-monthly intervals from 200-m transects. RESULTS: The flock was Se-deficient, as the mean initial concentration of Se in the blood of ewes was 182 (SE 20.3) nmol/L. Compared with untreated controls, all doses significantly (p < 0.01) increased concentrations of Se in the blood of ewes for at least 300 days. Selenium concentrations in milk were likewise increased throughout lactation, as were those in the blood and liver of lambs. The mean concentration of vitamin B12 in the serum of ewes was initially > 1,000 pmol/L, but this decreased within 28 days to < 460 pmol/L. Treatment with the 5-ml and 4-ml doses raised serum vitamin B12 concentrations of ewes for at least 176 days (p < 0.01), while their lambs had significantly greater concentrations of vitamin B12 in serum and liver for less than 37 days after birth. Tissue concentrations and duration of elevation of both vitamin B12 and Se were proportional to the dose administered. The mean concentrations of Se and cobalt (Co) in the pastures were 32 and 74 microg/kg dry matter (DM), respectively. CONCLUSIONS: Injecting ewes from a Se-deficient flock 4 weeks prior to mating with 48 or 60 mg Se and 12 or 15 mg vitamin B12 increased and maintained the Se status of ewes for at least 300 days, and of their lambs from birth to weaning. The vitamin B12 status of ewes was increased for at least 176 days and that of their lambs for less than 37 days. Due to the proportional nature of the response to increasing dosage, the dose rate of the formulation tested can be adjusted according to the severity of Se and Co deficiency in a flock. CLINICAL SIGNIFICANCE: A single subcutaneous injection of vitamin B12 + Se administered pre-mating to Se-deficient flocks is likely to prevent Se deficiency in ewes and their lambs until weaning, as well as increase the vitamin B12 status of ewes and their lambs until 5 weeks after lambing.     

Clinical and pathological studies in adult sheep and goats experimentally infected with Wesselsbron disease virus

The clinical symptoms and pathology in 33 adult sheep and 31 adult goats experimentally infected with Wesselsbron disease virus are described. There was moderate to severe hyperthermia in most animals, but no other clinical signs of disease or deaths were recorded. Eleven sheep and 6 goats were sacrificed for pathological studies at various stages during the febrile response. The macroscopic and microscopic lesions in these cases are described. Microscopic studies revealed that the liver was consistently affected and showed small foci of necrosis. These were sparsely distributed and associated with a marked localized Kupffer cell response ("retothelial nodules"). In addition, acidophilic bodies and small groups of necrotic hepatocytes were evident in some lobules. Apart from the hepatic lesions, mild to moderate pyknosis and karyorrhexis of lymphocytes were seen in the spleen and lymph nodes. This report also compares the microscopic lesions in the livers of adult sheep and goats with those of new-born lambs for Wesselsbron disease as well as with those reported for Rift Valley fever in adult sheep.     

WHITE LIVER DISEASE OF SHEEP

SUMMARY Outbreaks of ovine white liver disease (WLD) on 7 farms in eastern Victoria were investigated. Most occurred in late spring and mainly affected lambs 3 to 6 months old, with a morbidity of 20 to 100% and mortality of 8 to 15%. Clinically affected lambs showed illthrift, emaciation and bilateral, serous, ocular discharge. Clinical pathology showed mild anaemia, elevated serum liver enzymes (GGT, OCT, AST) and low levels of serum vitamin B12. Grossly, the livers were pale, fatty and friable; microscopically there was parenchymal fatty change, bile duct proliferation and ceroid pigmentation. Liver cobalt values were consistently low (mean 0.4 ± 0.4 μmol/kg D.W.). Levels of cobalt in pasture from 2 properties were very low (0.34 μmol/kg D.W.). The diagnosis of white liver disease was made on the basis of clinical features, specific liver pathology and low cobalt status. Treatment trials established that cobalt injections or oral bullet administration resulted in clinical improvement, significant weight gains, and improved serum vitamin B12 levels. WLD did not recur in previously affected sheep using these treatments. However, when blocks containing cobalt were available continuously, WLD recurred 2 years after the initial outbreak.     

The efficacy of a subcutaneous injection of soluble Vitamin B12 in lambs

AIMS: To assess the efficacy of a soluble Vitamin B12 injection in lambs by measuring changes in the serum and liver Vitamin B12 concentrations. METHODS: Thirty-six lambs were injected subcutaneously with 2 mg of soluble Vitamin B12 while another group of 36 served as untreated controls. Blood and liver biopsy samples for Vitamin B12 determinations were collected just before the injection and at days 1, 2, 5, 8, 16, 24, 30 and 45. RESULTS: The serum Vitamin B12 concentrations of the Vitamin B12 treated lambs increased rapidly compared to the untreated lambs. Concentrations peaked at day 2, decreased rapidly to day 8, and then decreased more slowly until day 24 when there were no longer differences between the groups. Liver Vitamin B12 concentrations of the Vitamin B12 treated lambs were significantly greater over days 8-24. CONCLUSION: A subcutaneous injection of 2 mg of soluble Vitamin B12 was effective in increasing and maintaining the Vitamin B12 status of lambs for about 24 days. CLINICAL SIGNIFICANCE: This Vitamin B12 product is only effective for preventing cobalt deficiency in lambs for about 4 weeks.     

Suspected photosensitisation in lambs grazing birdsfoot trefoil (Lotus corniculatus)

Suspected photosensitisation occurred in three groups of lambs grazing birdsfoot trefoil (Lotus corniculatus c.v. Grasslands Goldie). In one group, sucking lambs aged about 10 weeks, grazing birdsfoot trefoil, developed skin lesions while lambs of a similar age and from the same flock grazing lucerne (Medicago sativa) or a mixed sward of both species showed no signs of photosensitisation. Affected lambs had lesions on their backs and ears. In a few animals the tips of the ears were shortened by 2-3 cm. In the affected lambs, serum liver enzymes (gamma-glutamyltransferase, glutamate dehydrogenase), bilirubin and serum Vitamin B12 levels were within the normal range. At necropsy, no significant pathological changes were detected in the liver and histological changes in the skin were consistent with primary photosensitisation. In the second group, three of 80 weaned lambs grazing the same birdsfoot trefoil at a restricted intake were affected in the same manner as the first group. In the third group, 15 animals from 28 sets of sucking twin lambs were also affected. In only two sets of twins were both lambs affected. None of the ewes grazing with the lambs in the first or third groups showed any clinical signs of photosensitisation.     

Toxoplasmosis in a flock of sheep: some investigations into its source and control

Toxoplasmosis was thought to be a minor problem on a lowland sheep farm purchasing some 200 ewe lambs annually. Serological investigations and production records suggested a more substantial problem with most of the ewe lambs seroconverting during their first pregnancy, many while still at grass and receiving no supplementary food. Only 60 live lambs were produced per 100 ewe lambs tupped. It was known that cats occasionally inhabited the sheep houses, from which straw bedding was spread onto the pastures after lambing. Trials over two years with ewe lambs grazing either 'clean' or 'dirty' pastures indicated that the straw bedding was the most likely source of infection. Serial serological studies not only defined the time of infection but also showed that the ewe lambs could be kept free of infection and produce more live lambs; 58 live births came from 81 'clean' ewe lambs compared with 21 from 50 'dirty' ewe lambs.     

Acute respiratory distress syndrome (ARDS) in lambs. Clinical and pathoanatomical investigations

In the South-Western part of Norway, lambs of the Old Norwegian short tailed breed (Spael) and crosses with the Dala breed sometimes develop an Acute Respiratory Distress Syndrome (ARDS) shortly after they have been moved onto lush aftermath grazings from mountain pastures. This article covers the symptoms and pathoanatomical findings in lambs affected with ARDS (Table I). The lambs acquired ARDS 18-72 hours after change of pasture. Heavy dysphne, frothing at the mouth, elevated temperature (greater than 41 degrees C), tachycardia, urination and ruminal atony were striking symptoms (Table II). In the early phase of the disease the lambs were often in a tranquil state, depressed, sometimes atactic, and it seemed that they went into the overt dysphneic phase on exposure to physical stress. Morbidity was 1.4%, mortality 36%. Post mortem findings included frothy contents in the airways, heavy congestion and oedema in the lungs which also had emphysematous areas, subepicardial petechiae, varying degree of mottling of the myocardium, and also varying degree of paleness and spottyness of renal cortices. The lungs showed extensive focal alveolar and interstitial emphysema, septal congestion, alveolar oedema, partial collapse, and accumulations of polymorphonuclear leucocytes in vascular beds. Later, fibrillar material was found in the alveoli, alveolar macrophages accumulated, and interalveolar septa thickened because of increased fibromuscular tissue and mononuclear cells (Fig. 1, A-D). Alveolar epithelial hyperplasia was not seen in any stage. Four lambs were moderately infected with lungworms (D. filaria), three in the prepatent, one in the patent phase. Histopathological changes in other organs included granular degenerations of myocardial threads, and development of a glomerulonephritis and focal interstitial nephritis (Fig. 1, E-F). This disease entity (ARDS) in lambs seems to be unknown in literature. The disease is compared with other known diseases in ruminants. Etiology is so far unknown. Possibilities of sudden ruminal histamine formation coinciding with a hypersensitivity reaction is discussed.     

Kleingrass (Panicum coloratum L.) poisoning in sheep

Twenty-four lambs grazing pastures of Panicum coloratum developed photosensitization secondary to hepatic dysfunction. Lesions were necrosis of scattered hepatocytes, obstruction of small bile ducts and bile canaliculi by small aggregates of birefringent crystals, and accumulation of birefringent crystals in phagocytes within sinusoids. The number of crystals in livers of affected sheep varied, depending on the amount of time of exposure to toxic plants and severity of hepatic abnormalities. Crystals in the liver were soluble in acidified ethyl alcohol, acetic acid, pyridine, chloral hydrate, and methanol, but not in xylene, petroleum ether, diethyl ether, acetone, water, or cold ethyl alcohol. Crystals were not stained by oil red O. There was necrosis of epithelial cells in renal distal convoluted tubules, papillary muscles of the heart, and the adrenal cortex. Lesions of Panicum coloratum-associated disease are similar to those associated with photosensitization induced by Tribulus terrestris, Agave lecheguilla, and Nolina texana.