Nonprotein nitrogen-induced ammonia toxicosis and ammoniated feed toxicity syndrome.

In spite of all the reports and work done, the ammoniated feed toxicity syndrome still is quite a mystery. Given its enigmatic cause, prevention is our only current means of control. The data that is recorded from each new episode, however, may help to piece together the exact mechanism so that one day it can be understood and treated.

Tremorgenic syndromes in livestock.

Grasses that are essential components of livestock grazing programs sometimes are the source of tremorgenic toxicants to the animals consuming them. Morbidity can be high but mortality need not be if management closely observes the cattle daily and removes them at first sign of trouble. Specific treatment generally is not available nor needed. Survivors recover completely within a few days or weeks, except in chronic phalaris poisoning, where sheep and cattle may die after prolonged illness--or at least not make an economical recovery. Certain poisonous plants are responsible for tremorgenic signs in livestock and horses. White snakeroot and rayless goldenrod pose a public health risk to individuals who might drink milk from a goat or cow grazing toxic amounts of these weeds. Poisonous weeds and trees often are a local or regional problem, and often are seasonal. A veterinarian new to the area who has a food animal practice should seek out information relative to poisonous plants, nutritional deficiencies, and diseases endemic to the practice area. The ability of certain fungi to produce toxic metabolites in feed-stuffs creates the potential for tremorgenic or other types of toxicosis in most classes of livestock. Wet grain byproducts from ethanol production and other processes can provide the right culture media for fungi.

Caval syndrome in a Dirofilaria immitis-infected dog treated with dichlorvos.

In the dog of this report, lesions found were compatible with death attributable to acute circulatory collapse induced by caval syndrome and compounded by microfilarial death. Hepatic centrilobular hemorrhage and necrosis were suggestive of circulatory collapse, renal hemosiderosis was suggestive of disseminated intravascular coagulopathy, and multifocal subacute hepatic inflammation associated with microfilariae was similar to lesions attributed to microfilarial death. Treatment with dichlorvos may have precipitated these events. Previous descriptions of dichlorvos toxicity in microfilaremic dogs have suggested that death is attributable to shock, but pathogenic mechanisms have not been established. Although generalizations from a single case must be made with caution, lesions in this dog suggest that toxic effects may be mediated through effects on adult and larval heartworms.

Detection of antibodies to platelets and erythrocytes during infection with haemorrhage-causing Trypanosoma vivax in Ayrshire cattle.

Ayrshire cattle, which were infected with a stock of Trypanosoma vivax from Galana, Kenya, which produced haemorrhagic disease, were examined for the presence of antibodies to erythrocytes and platelets. Antibodies to normal erythrocytes and platelets were detected in the plasma of infected animals using the enzyme-linked immunosorbent assay (ELISA). The antibodies were detectable following the first peak of parasitaemia (10-15 days after infection) and antibody activity was maximal 30-35 days after infection. Plasma from cattle, taken 32 days after infection, precipitated radiolabelled proteins from autologous platelets and, less efficiently, from autologous erythrocytes. Fluorescence-activated cell sorter (FACS) assays demonstrated that erythrocytes and platelets from infected cattle bound IgM and IgG in vivo, and that both normal blood cell types could adsorb these antibodies following incubation in plasma from infected animals. Complement (C3) was similarly adsorbed to erythrocytes during infection. Antibodies adsorbed to infected erythrocytes could be eluted and the eluted antibodies bound to normal erythrocytes, as detected by immunofluorescence, but they did not react with the infecting trypanosome. It is hypothesised that although anti-blood cell antibodies may not be the primary cause of the severe anaemia and thrombocytopaenia which accompany the haemorrhagic syndrome, they could play an important role in the maintenance of these signs of disease, adversely affecting the outcome of T. vivax-associated haemorrhagic disease in the field.

Wasting pig syndrome (WPS) in weaners--treatment with amperozide.

Social and environmental stressors during the critical period of weaning frequently affect not only performance but also the health status of piglets. Pigs unable to cope with the changes associated with weaning develop a condition characterized by slowing of growth and a listless or unthrifty appearance, known as the wasting pig syndrome (WPS). In the present investigation a total of 100 4-week-old wasting pigs were studied. The pigs were divided randomly into 10 pens (10 animals per pen). Half the number of pigs were treated orally with amperozide (2.5 mg/kg body-weight), a psychotropic drug shown to modify emotional behaviour in response to social stress. Control groups were treated with long-acting oxytetracycline and vitamins (A + D3 + E). There were significant improvements in average daily weight gain (P less than 0.05) and feed conversion ratio (P less than 0.01) in amperozide-treated pigs compared with controls. Furthermore, there was a significant reduction (P less than 0.05) in mortality in amperozide treated groups. Within 2 weeks following amperozide treatment the clinical signs of the WPS had disappeared and the pigs grew at the same rate as normal healthy pigs.

Haemorrhagic lesions resulting from Trypanosoma vivax infection in Ayrshire cattle.

Infection of Ayrshire cattle with a stock of Trypanosoma vivax from the Galana Ranch, Kenya, resulted in an acute disease characterised by profound anaemia and haemorrhage, which reached maximum severity between 3 and 5 weeks after infection. Bleeding from the ears, nose and rectum occurred. At necropsy, petechial and ecchymotic haemorrhages were widespread, but were particularly severe in the gastrointestinal tract. In confirmation of the gross findings, congestion, haemorrhage and degenerative changes in most tissues and organs were found histologically. Thrombi were seen in the lymphatic vessels and clots of fibrin were present in the ventricles of the brain. The anaemia was a consequence of frank blood loss through haemorrhaging, exacerbated by erythrophagocytosis of deformed red blood cells, whose occurrence was indicative of microangiopathic changes. Animals were euthanised between 23 and 36 days after infection when they became recumbent with PCV values as low as 9%. There is no doubt that animals affected by this syndrome in the field would die within a few weeks of infection, if left untreated.

Physiological evaluation of diuresis in commercial broiler breeders.

A physiological investigation on an outbreak of diuresis syndrome in commercial broiler breeder hens was carried out. Daily water consumption increased 4-fold and daily manure wet weight increased two-fold in affected hens. 2. The syndrome did not have a genetic basis. It was associated with kidney dysfunction which, once acquired, was not alleviated by changing the diet, the drinking water, or the environment. Diuresis ceased when water intake was restricted and returned when water was again made freely available. 3. The syndrome was not caused by nephrogenic diabetes insipidus or diabetes mellitus. Key changes in kidney function associated with diuresis included: increased urine flow, decreased urine osmolality, reduced glomerular filtration rates, increased fraction of the glomerular filtration rate excreted as urine and decreased urinary hydrogen ion concentrations. 4. Preliminary histopathological findings and the physiological patterns of kidney dysfunction indicated that the diuresis syndrome was associated with permanent kidney damage, probably caused by the Arkansas strain of infectious bronchitis virus.

Taurine deficiency syndrome in cats.

Taurine deficiency occurs in a large number of cats fed unfortified commercial diets. Deficiency arises because cats are unable to absorb all the taurine in processed diets and/or are unable to synthesize the deficit between absorption and requirement, which makes taurine an essential amino acid for cats. Taurine-depleted cats develop retinal degeneration, cardiomyopathy, altered white-cell function, and abnormal growth and development. Taurine deficiency is best estimated from the plasma-taurine concentration, with values less than 30 mumol/l considered deficient.

Feline kaliopenic polymyopathy/nephropathy syndrome.

The prevalence of hypokalemia in cats has probably been underestimated until recently. Like many other "contemporary" diseases, this syndrome is probably not new; however, it is now more easily recognized because of the identification of associated dietary and disease risk factors, clinical signs, and laboratory abnormalities, which have been linked to the expected pathophysiology of potassium depletion in the cat.

Sprague Dawley rat mutant with tremor, ataxia, tonic immobility episodes, epilepsy and paralysis.

A spontaneous neurological mutation was detected in a colony of Sprague Dawley rats. The animals developed a progressive neurological syndrome characterized by tremor (which appeared at the age of 1 month), ataxia (at 4 months), immobility episodes (after 5-6 months), audiogenic seizures and hindlimb paralysis (after 10 months). Cross breeding experiments indicate that this is an autosomal recessive mutation, which we have named taiep subline.

Neuroradiographic diagnosis and surgical repair of tethered cord syndrome in an English bulldog with spina bifida and myeloschisis.

A 3-month-old English Bulldog had excretory incontinence and sensory deficits in the distribution of pudendal nerves. Noncontrast radiography, myelography, and computed tomography revealed spina bifida beginning at L7, an expanded subarachnoid space caudal to L7, and a taut, thick filum terminale. Microsurgical exploration of the lumbosacral spine confirmed the presence of a tethered cord, and the filum terminale was transected. The spinal cord immediately migrated cranially about 1 cm. Although some sensory improvement was evident during a 2-week postoperative period, the dog was euthanatized. Postmortem examination confirmed spina bifida and atrophy of sacral nerve roots and perineal muscles, thoracic hemivertebrae, and hydrocephalus.

Pathophysiology of navicular syndrome.

Navicular syndrome is a degenerative disorder of the distal half of the flexor surface of the proximal sesamoid bone that is predisposed by faulty foot conformation. In horses that become symptomatic, the faulty conformation results in sustained application of nonphysiologic pressure by the deep digital flexor tendon against the flexor cortex of the bone. This force stimulates an intense bone remodeling response in order to attenuate the pressure. An unfortunate sequela of this response is active hyperemia and edema formation in the medullary cavity of the bone. The edema is organized by fibrous tissue resulting in venous entrapment, venous hypertension, vascular bone pain, and the onset of clinical signs.

Diagnosis and treatment of the navicular syndrome in horses.

Navicular syndrome can be treated in a variety of ways. This is related to the fact that it has a variety of causes. Prognostically, most horses will improve with treatment. One can expect about 50 per cent of the horses to become useably sound for 1 year, no matter what treatment is used. The disease is progressive, and affected horses eventually will need to be retired because of lameness. The author's therapeutic approach is to utilize shoeing as the primary therapy. Shoeing is performed to correct structural problems and to ensure that shoeing is physiologically sound. Nonsteroidal anti-inflammatory drugs are not used unless radical changes have been made in the shoeing. In cases of confirmed distal interphalangeal joint synovitis, either sodium hyaluronate or polysulfated glycosaminoglycans will be used in conjunction with shoeing. In cases where decreased circulation is documented, isoxsuprine hydrochloride will be administered if shoeing alone has not improved the horse within 6 weeks. If therapy does not improve the horse within 6 to 12 weeks, palmar digital neurectomy is recommended.

Focal ulcerative ileocolitis with terminal thrombocytopenic purpura in juvenile cotton top tamarins (Saguinus oedipus).

A newly recognized syndrome characterized by an acute focal ulcerative ileocolitis, anemia and thrombocytopenic purpura in five juvenile cotton-top tamarins is described. The presentation and morphology of this syndrome is distinct from any other reported gastrointestinal disease reported in tamarins. Traditional etiologies such as viruses, ingested toxins, Campylobacter, Salmonella and Yersinia and Clostridium difficile are not considered likely etiologic agents. Nontraditional etiologies such as anaerobes or pathologic strains of Escherichia coli are now being considered. This syndrome is of potential significance to ongoing research into the etiology of idiopathic tamarin colitis.

Breed differences in plasma calcium, phosphorus and magnesium concentrations of Merino, Dohne Merino and S.A. Mutton Merino sheep with relation to the bent-leg syndrome.

Plasma calcium, phosphorus and magnesium concentrations were determined in ewes and their single and twin lambs from birth for 120 days in Merino, Dohne Merino and South African Mutton Merino sheep. Mineral concentrations as well as the plasma calcium: phosphorus ratio were compared between breeds. Throughout the experimental period, plasma calcium and phosphorus concentrations were higher in both single and twin lambs than in the ewes of all 3 breeds. No breed differences in plasma calcium concentrations were found. Animals of the S.A. Mutton Merino breed had significantly higher (P less than 0.05) plasma phosphorus concentrations than the other 2 breeds. The plasma Ca:P ratio in the Merino and Dohne Merino ram lambs was approximately 1.1:1 and in the S.A. Mutton Merino 0.9:1. This converse plasma Ca:P ratio found in both the S.A. Mutton Merino ewes and lambs is believed to result in an induced plasma ionised calcium deficiency which leads to improper calcification of bone. This is believed to be a contributing factor in the bent-leg syndrome. No difference was recorded in body mass between ram lambs suffering from the bent-leg syndrome and unaffected ram lambs. Plasma magnesium concentrations were not affected by breed or age of the animals.

[The fat mobilization syndrome in guinea pigs (Cavia porcellus L.)]. / Untersuchungen zum Fettmobilisationssyndrom am Meerschweinchen (Cavia porcellus L.).

Feeding experiments were applied to 82 guinea pigs, different by age, sex, and stage of reproduction, and showed that high-energy feeding and subsequent feed withdrawal could trigger off with high probability a fat mobilising syndrome with clinically manifest ketosis in animals in gravidity and lactation or subclinical ketosis in all non-gravid individuals. High-energy or restrictive feeding alone did not cause in guinea pigs any disease along the lines of gravidity toxicosis. Aspects relating to aetiological and pathogenetic comparability with ruminants are discussed in some detail.