Blindness and convulsions associated with vitamin A deficiency in feedlot steers

Blindness and convulsions were the predominant clinical signs in a group of feedlot steers inadvertently fed a vitamin-A deficient diet. Although vitamin A had been added to the feed at the time of preparation, it was believed that the vitamin A had been destroyed by heat, humidity, and minerals mixed in the feed. Feedlot heifers fed the same high-grain diet were clinically normal, and one heifer from which a blood sample was obtained had normal serum vitamin A content. The ingestion of sparse grasses and weeds found along the fence row of the heifers' pens was thought to have provided sufficient vitamin A to these animals. This episode demonstrated the importance of monitoring vitamin A and vitamin A precursor concentrations in stored feeds, especially those stored under adverse conditions and those fed to animals ingesting only a high-grain diet.     

Cerebellar abiotrophy in crossbred cattle

Cerebellar abiotrophy affected 9 of 74 calves sired by a Poll Hereford bull over 2 successive calving seasons. The disease was characterised by episodes of recumbency and ataxia, with hypermetria and wide base stance. Clinical signs commenced between birth and 8 months of age. Two calves which were affected first at 8 months of age recovered clinically 9 months later. Histological lesions were found in the cerebellar cortex of 7 calves and consisted of segmental degeneration and loss of Purkinje cells, and axonal swellings. The clinical signs and pathological findings were consistent with bovine familial convulsions and ataxia, which has not been described previously in Australia. The clinical signs were not attributable to the lesions observed in the cerebellum and an underlying electrophysiological abnormality is proposed. The aetiology of the condition is probably genetic and appears to have a multifactorial basis.     

Hypovitaminosis A in feedlot cattle

Hypovitaminosis A was diagnosed in a group of feedlot cattle that had been fed a diet low in carotene for 18 months. The primary signs of disease in the cattle were poor weight gain, ataxia, convulsions, night blindness, and total blindness. Serum vitamin A concentrations were used to confirm the diagnosis. The cattle were treated orally and intramuscularly with vitamin A, and the less severely affected herd members recovered rapidly.     

Cerebellar cortical degeneration in three English bulldogs: clinical and neuropathological findings

This case report describes the clinical and neuropathological findings in three young English bulldogs affected by cerebellar cortical degeneration. The dogs, born from the same parents, were presented with clinical signs indicating progressive cerebellar dysfunction: a wide-based stance, severe cerebellar ataxia characterised by marked hypermetria, spasticity, and intention tremors of the head and trunk with loss of balance. On histopathological examination, lesions were confined to the cerebellum and consisted of diffuse degenerative cortical lesions, and there was a loss of Purkinje and granule cells. The history, clinical signs and neuropathological findings confirmed the diagnosis of cerebellar cortical degeneration. To the authors' knowledge, this is the first report of cerebellar cortical degeneration in the English bulldog.     

Encephalopathy caused by Talisia esculenta intoxication in pregnant ewes and their newborn lambs

An outbreak of acute encephalopathy occurred in pregnant ewes and their newborn lambs associated with consumption of Talisia esculenta fruits and bark. Clinical signs in 5 adult pregnant ewes included drooling, bloat, tachypnea, depression, ataxia, body shaking, difficulty in rising, and recumbency. Three neonatal lambs born to some of those ewes had similar clinical signs. No significant gross abnormalities were observed on autopsy. Histologically, neuronal necrosis, axonal and dendritic swelling, and loss of Purkinje neurons were observed in the cerebellum. The observation of similar neurologic clinical signs and lesions in pregnant ewes and their neonatal lambs suggests that the toxic principle of T. esculenta crosses the placenta and reaches the fetus.     

Brain, liver and plasma unsaturated aldehydes in nutritional encephalomalacia of chicks

Vitamin E deficiency and linoleic acid-feeding lead to nutritional encephalomalacia (NE) in chicks, affecting the cerebellum exclusively. The relevance of lipid peroxidation (LPO) products to the pathogenesis of the disease was studied. Laying hens received a diet low in vitamin E. Resulting chicks were assigned to four groups fed either with linoleic (C18: 2n-6) or linolenic (C18: 3n-3) acid together with 1 or 50 p.p.m. vitamin E. Nine days post-hatching NE occurred in the vitamin E-deficient group fed linoleic acid. With each chick showing NE, a healthy one from all four groups was killed. Unsaturated aldehydes were determined in plasma, liver, cerebrum and cerebellum. Results underlined that the type of dietary fat is decisive for the aldehyde pattern. In the liver of linoleic acid-fed animals total aldehydes were increased. Diseased animals had increased aldehydes stemming from n-3 fatty acids. In plasma, vitamin E deficiency led to higher malondialdehyde and OH-nonenal concentrations. In brain, neither vitamin E deficiency nor NE were accompanied by increased aldehyde concentrations. In consequence a direct role of unsaturated aldehydes for the development of NE in the cerebellum is not probable.     

The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep.

The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep.     

The effect of a homologous bacterin given to sows prefarrowing on the development of Glässer's disease in postweaning pigs after i.v. challenge with Haemophilus parasuis serotype 5

The trial was carried out to evaluate the impact of maternal antibodies on the development of Gl?sser's disease after i.v. exposure of weaned pigs with a homologous serovar of Haemophilus parasuis (HPS). Two groups of weaned pigs were formed. Group one VI (n = 10): born to vaccinated sows, weaners i.v. challenged one week postweaning and euthanatized 14 days postweaning. Group two NVI (n = 10 wearners): born to non vaccinated sows, i.v. challenged one week postweaning euthanatized 14 days postweaning. One week postweaning all weaners were i.v. inoculated with HPS serovar 5. The following parameters were evaluated: clinical signs (depression, centralnervous signs, fever, lameness), macroscopic lung, pleura, peritoneum, liver and joint changes, and mortality. All trial sows were HPS seronegative prior to vaccination. The HPS vaccinated sows were proven seropositive on day 3 p.p. (values > 0.24), the non vaccinated ones were tested seronegative (values < 0.23). The progeny of sows vaccinated prefarrowing with two doses of HPS serovar 5 bacterin were partially protected against HPS caused clinical and pathological signs. The majority of clinical signs as fever, depression, recumbency, lack of response to verbal stimuli and lameness showed significant (P < 0.05) milder clinical symptoms in VI than in NVI animals. Respiratory signs (P = .169) and involvement of the central nervous system as ataxia, muscular tremor, incoordination of hind legs and convulsions (P = 1) showed no significant differences between the groups. Except lesions of pericard (VI vs. NVI, P = .14) and pleura (VI vs. NVI, P = .14) there were significant (P < 0.05) macroscopic differences at necropsy in lung, liver, joints and cerebrospinal fluid between the offspring of vaccinated sows and the ones of non vaccinated dams. No HPS were isolated from the nasal mucosa of the pigs prior to inoculation. HPS serovar 5 was recovered at necropsy from the nasal mucosa of all pigs in both groups. One pig from group VI presented in all examined organs the presence of HPS serovar 5. The remaining animals in group VI revealed in lung, pericard, pleura, liver, joints and cerebrospinal fluid no presence of HPS. The rate of isolation between VI and NVI groups revealed a significant (P < 0.05) difference. All the survived piglets of group NVI showed positive ELISA titres against HPS serovar 5 (values > .24). The piglets that died or were euthanatized before the end of the study have not been subjected to ELISA serological testing. One piglet died in group VI before the end of the study. Non of the remaining animals in group VI showed seroconversion to HPS serovar 5. Implications: Vaccination of sows did not influence the colonisation of nasal mucosa, but progeny of sows vaccinated prefarrowing with two doses of HPS serovar 5 bacterin were partially protected against HPS caused diseases.     

Clinical Parelaphostrongylus tenuis infection in two captive American bison (Bison bison)

CASE DESCRIPTION: 2 juvenile (17 and 19 months of age) male American bison (Bison bison) were examined because of acute bilateral hind limb weakness and ataxia; 1 animal also had urinary incontinence. TREATMENT AND OUTCOME: Given the clinical signs and rapid deterioration in the condition of these 2 animals, obtaining a definitive diagnosis was considered essential to minimizing the risk of disease in the remaining bison herd and among other animals at the facility. Therefore, both affected animals were euthanized. At necropsy, no gross abnormalities were seen. Histologic examination of sections of the brains from both animals revealed mild to moderate multifocal aggregates of eosinophils and mononuclear cells in perivascular regions of the meninges and gray matter of the cerebrum, cerebellum, and brainstem. Systematic examination of multiple sections of brain and spinal cord revealed evidence of nematode sections and aberrant parasite migration. CLINICAL RELEVANCE: Findings suggested that CNS migration of Parelaphostrongylus tenuis in American bison may cause clinical signs. These findings have implications for the management of captive bison and free-ranging bison sharing ranges with white-tailed deer (Odocoileus virginianus), the definitive host, and elk (Cervus elaphus canadensis).     

The use of diazepam and methocarbamol in the treatment of toxaphene poisoning in a Bangal tiger.

A 12-year-old female Bengal tiger was presented with clinical signs of acute chlorinated hydrocarbon poisoning and a history of recent consumption of food contaminated with toxaphene. Hyperreflexia and periodic convulsions were controlled by initial intramuscular injections of 30 mg diazepam and 2 g methocarbamol, followed at 6-hour intervals with intramuscular injections of 30 mg diazepam each, for 2 additional treatments. Following the initial treatment, hyperreflexia and convulsions did not recur.     

Age distribution of animals persistently infected with bovine virus diarrhea virus in twenty-two Danish dairy herds.

The objectives of this study were to compare the age distribution of animals persistently infected (PI) with bovine virus diarrhea virus (BVDV) in 12 herds with clinical BVD compared to ten herds without clinical BVD and to examine the incidence of PI calves born after the oldest PI animal. Blood samples from all animals were tested for bovine virus diarrhea virus and antibodies. In five herds, blood samples were obtained from calves born after the whole herd had been tested. All calves born by PI dams were also blood tested. In herds with clinical BVD the median age of PI animals was 248 days and in herds without clinical BVD the median age was 144 days. There was no significant difference between the age of PI animals in herds with clinical BVD compared to herds without clinical BVD (p = 0.48) suggesting similar epidemiology of the occurrences of PI animals in the two herd categories. Thereafter, all herds were used to study the incidence of PI animals. A total of 129 PI animals were found. In ten herds with 72 PI animals the age range of PI animals was more than six months. In these herds 26.3% of the PI animals were born within the first two months after birth of the oldest PI animal, no PI animals were born 2- less than 6 months, 52.7% were born 6- less than 14 months, 6.9% were born 14- less than 22 months and 13.9% (all born by PI dams) were born later than 22 months after the oldest PI animal.(ABSTRACT TRUNCATED AT 250 WORDS)     

Feline Temporal Lobe Epilepsy: Review of the Experimental Literature

Accumulating evidence suggests that epileptic seizures originating from the temporal lobe (TL) occur in cats. Typically, affected animals have clinically focal seizures with orofacial automatisms including salivation, facial twitching, lip smacking, chewing, licking, and swallowing. Motor arrest and autonomic and behavioral signs also may occur. Many affected cats have magnetic resonance imaging (MRI) changes within the hippocampus or histopathologically confirmed hippocampal sclerosis or necrosis. From the 1950s to the 1980s, cats frequently were used as animal models for neurophysiological experiments and electrophysiological studies, from which important basic knowledge about epilepsy originated, but which has been rarely cited in clinical veterinary studies. These studies were reviewed. Experimental research on cats showed the widespread anatomical connections among TL structures. The ictal clinical signs originating from the hippocampus, amygdala, or lateral temporal cortex are similar, because of their dense interconnections. The ictal signs can be divided into autonomic, somatic, and behavioral. For research purposes, a 6‐stage system was established, reflecting the usual sequential progression from focal to generalized seizure: attention response (1), arrest (2), salivation, licking (3), facial twitching (4), head turning or nodding (5), and generalized clonic convulsions (6). Knowledge of this data may help in recognizing low‐stage (stage 1 or stage 2) epileptic seizures in clinical practice. Early experimental research data are in accordance with recent clinical observations regarding ictal clinical signs of TL epileptic seizures in cats. Furthermore, the research data supports the idea that TL epilepsy represents a unique clinical entity with a specific seizure type and origin in cats.     

The toxicity and kinetics of larkspur alkaloid,methyllycaconitine, in mice

Larkspur poisoning sporadically kills from 5 to 15% of the cattle on North American mountain rangelands. Of the 40 different diterpenoid larkspur alkaloids, the one that is thought to be responsible for much of the toxicity has been identified as methyllycaconitine (MLA). Little is known of MLA toxicokinetics or excretion. The purpose of this study was to further characterize the clinical effects of MLA toxicity in mice and determine the toxicokinetics of MLA excretion. Eight groups of mice were dosed intravenously with 2.0 mg/kg of BW of MLA, killed, and necropsied at 0, 1, 2, 5,10,15, 30, and 60 min after injection. Treated animals were reluctant to move, trembled, and developed dyspnea, muscular twitches, and convulsions. Within several minutes, the clinical signs abated and behavior slowly returned to normal over approximately 20 min. At necropsy serum, brain, liver, kidney, and skeletal muscle were collected and frozen. Blood and tissues were extracted and analyzed for MLA with HPLC and electron spray mass spectrometry. Blood MLA elimination followed a normal biphasic redistribution and excretion pattern (r = 0.99) with a K of elimination of 0.0376 and half-life of 18.4 min. Other tissues had similar clearance rates. These data indicate the MLA is rapidly distributed and excreted. In mice, the clinical effects of poisoning seem to affect the central nervous system, causing dyspnea and "explosive" muscular twitches and convulsions. Because livestock commonly eat larkspur at subclinical doses, they are likely to have larkspur alkaloids in many tissues. These results suggest that animals exposed to larkspur should rapidly excrete MLA (within several hours) and that the residues in animal tissues are not likely to be a problem if animals are given several days to allow toxin clearance.     

Hypervitaminosis D in fur-bearing animals.

Investigations concerning the effect on fur-bearing animals of large doses of vitamin D3 were carried out. The material comprised 62 animals in all--10 silver foxes, 17 blue foxes and 35 mink (Table II). Daily doses of 5 IU vitamin D3/g body weight for two months did not produce clinical symptoms in the foxes. However, a short while after the dose was increased to 10 IU, the animals showed loss of appetite, had difficulty in moving, were apathetic and developed dark coloured faeces. Analysis of blood serum showed markedly raised calcium values (Table III). Calcium deposits were demonstrated in the kidneys and in some cases also in the musculature, gastric mucosa, bronchi and the larger blood vessels. No abnormal signs were shown by 30 mink which received 0.6--0.7 IU vitamin D3/g body weight for five months. PM findings were normal.     

Intra-uterine Infection with Babesia bovis in a 2-day-old Calf

Infection with Babesia bovis was diagnosed in a 2-day-old female calf apparently transmitted in utero. The calf was born as the second calving to a cross-bred beef cow permanently on pasture. Diagnosis was based upon identification of B. bovis in peripheral blood smears and clinical signs which included fever, jaundice, pale mucous membranes and convulsions. Anaemia, leucocytosis, thrombocytopenia and lymphocytosis were noted at the febrile acute stage of the disease. The blood smears revealed evidence of regeneration of toxic neutrophils with a left shift, severe spherocytosis and high degree of basophilic stippling. Elevated concentration of aspartate aminotransferase, lactate dehydrogenase, and creatine kinase were also noted, and were probably the result of haemolysis, dehydration and muscle damage because of recumbancy. Elevated total bilirubin concentration following haemolysis resulted in jaundice. The neurological symptoms observed were probably caused by sludging of parasitized erythrocytes in the brain capillaries. The calf recovered following treatment with diminazene aceturate and the recovery was followed up clinically, haematologically and biochemically.     

Individual differences in the vitamin A metabolism of the order Carnivora--a review

Vitamin A transport in blood of most species in the order carnivora is fundamentally different from other animals and man. Very high levels of vitamin A in blood plasma of canines and mustelides are due to a high percentage of retinyl esters. These esters (basically retinyl palmitate and stearate) are transported nonspecifically bound to lipoproteins with very-low and low density lipoproteins representing the major fractions (about 70% of total vitamin A esters). A high percentage of retinyl esters could also be found in the families Ursidae, Procyonidae, Viverridae and Felidae in which total vitamin A in blood was low. In man and rat severe signs of vitamin A intoxication can be observed due to a similarly high percentage of nonspecifically bound vitamin A esters. No clinical or clinical-chemical signs of vitamin A intoxication were observed in the animals investigated. Because vitamin A esters are transported by lipoproteins, their blood levels are readily affected by dietary vitamin A supply as it is known to be the case for vitamin E. Furthermore, canines seem to be the only ones that excrete vitamin A as retinol and retinyl esters (basically retinyl palmitate) under physiological conditions with the urine. These fat-soluble metabolites of vitamin A are bound to a protein with a molecular weight between 50,000 and 125,000 Da which shows characteristics of a lipoprotein when subjected to ultracentrifugation or selective precipitation. Higher levels of vitamin A in organs and tissues, as well as the excretion of vitamin A with the urine, might be a consequence of the nonspecific binding of large amounts of retinyl esters to lipoproteins in blood.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pestivirus in cattle: experimentally induced persistent infection in calves

Twenty-two heifers were infected intranasally with non-cytopathic bovine viral diarrhoea virus (BVDV) between days 74 and 82 of pregnancy. All animals had developed serum antibodies against BVDV 5 weeks later. No clinical effects were seen in the heifers, and they all delivered a live calf. The newborn calves were generally small, appeared unthrifty as typical 'poor doers', and some developed secondary infections with diarrhoea and signs of respiratory disease. Eighteen of the 22 calves were born without antibodies against BVDV and were persistently infected (PI) with the virus. One was weak at birth and died the following day. Four calves were born with serum antibodies against BVDV and with no detectable virus. Three of these showed signs and/or pathological changes indicating disease in the central nervous system. Otherwise, there were no obvious clinical differences between these calves and the PI calves, nor were there any apparent significant differences in blood parameters between these groups. In general, the calves showed low gamma-globulin values and thrombocytopaenia, but moderately increased fibrinogen values and relatively normal lymphocyte numbers.     

Secondary effects caused by feed medication in swine

Giving medical feed to weanling pigs it is possible to produce a vitamin K-deficiency as a side effect, which is caused by destruction of the intestinal flora. In this investigation the effect of different drugs in a vitamin K-deficient diet on blood coagulation of weanling pigs was examined. In a first trial clinical symptoms of a vitamin K-dependent coagulation disorder could be seen in five from six animals after feeding a combination of sulfadimidine, tylosin, furazolidone and arsanilic acid. Animals showed haemorrhages, when they were housed on flatdecks as well as on concrete floor. This indicated that coprophagy plays no role in pigs for supply of vitamin K. Feeding these drugs in other combinations or one of the drugs alone caused no clinical signs in a second trial. Significant differences to untreated control pigs were found only in one group (sulfadimidine/arsanilic acid) for activities of coagulation factors. Other groups demonstrated only prolongation of clotting times in single animals. Pigs, which received sulfadimidine within their ration, were more often affected than other animals. In a third trial suckling pigs were treated over a period of three weeks with a drug combination used in the first trial to allow an adaptation of the intestinal flora. Same treatment after weaning was unable to produce any clinical symptoms, but led to distinct coagulation disorders in pigs treated before as well as in untreated animals. It is supposed that the development of a vitamin K-deficiency depends on faecal bacterial count and on the specific resistance of intestinal flora in individuals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Late onset cerebellar degeneration in a middle-aged cat

Cerebellar degeneration (abiotrophy) (CD) is a spontaneous and accelerated degeneration of one or several mature cerebellar neuronal cell populations and has been described in many domestic animals, especially in dogs, with numerous breed-related cases. In cats, CD is mentioned as a rare sporadic entity. Late onset CDs are exceptionally uncommon and only two cases are reported in young adults, both aged 18 months. This report describes clinical and pathological findings of a late onset feline CD in a 9-year-old male Persian cat. The cat was presented with a history of progressive ataxia lasting 2 years. Neurological examination revealed severe neurological deficits such as generalised and severe ataxia, hypermetria in all four limbs, and bilateral absence of menace response. The lesion was diffusely localised in cerebellum. On gross pathology, the cerebellum appeared of normal size and shape and kidneys were characterised by mild hyperaemia. Histologically, lesions were limited to the cerebellum and kidneys. In the cerebellum, all cerebellar folia of both hemispheres and the vermis were affected. Changes were characterised by severe and diffuse loss of Purkinje cells, loss of cellularity in the granular layer, mild astrogliosis associated with moderate hypertrophy of Bergmann's glia. Immunohistochemistry for feline parvovirus antigen revealed a negative result. Renal lesions consisted of chronic fibrosis associated with chronic interstitial nephritis. CD is a rare disease and occurs commonly in puppies or young animals, who are clinically normal at birth and usually develop neurological signs within a few weeks or months after birth. This report represents the first case of CD in a middle-aged cat.