Idiopathic hypersegmentation of neutrophils in a horse.
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Biomedical subjects
Publications and source records attributed to R H Whitlock.
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Control (.5% chloride) or low-chloride (.038% chloride) practical diets and low-chloride (.00038% chloride) well water were fed to male Holstein calves for 7 wk. Substantial alterations in characteristics of blood associated with acid-base balance developed in those fed the low-chloride diet. Along with reduced potassium in plasma, concentrations of chloride in synovial fluid, saliva, and plasma also were reduced. Solids in plasma, blood pH, packed cell volume, carbon dioxide pressure (PCO2) in blood, and bicarbonate were increased. Most of the changes in plasma occurred within 1 wk with little change thereafter, indicating an adaptation by the calves to the low-chloride diet. The adaptation by the low-chloride calves was primarily due to a tremendous reduction in urinary chloride excretion. Change in blood factors was insufficient to cause severe alkalosis in calves. The low-chloride diet had no significant effect on sodium absorption, retention, or distribution in body fluids. Potassium in plasma and aqueous humor were reduced in calves fed the low-chloride diet, but potassium concentrations in other body fluid were not affected significantly.
Potassium chloride and sodium chloride were infused into the reticulorumen of male Holstein calves, approximately 6 mo of age and 260 kg, at .29, .58, 1.15, 1.73, 2.31, or 2.88 g potassium per kilogram body weight or 1.35, 2.12, or 2.16 g sodium per kilogram in equal volumes of water. Paired controls were infused with water. Calves were monitored for physiological changes for 6 h at 15, 30, or 60-min intervals. Potassium and total solids of plasma and packed cell volume were increased at potassium doses greater than .29 g of potassium per kilogram body weight within 1 h after dosing. At the higher doses of potassium, sodium content of plasma increased about 1 h after the increase in plasma potassium. Respiration rates within a potassium treatment varied with respect to time after dosing, but generally they increased, and associated variables of carbon dioxide pressure, pH, and bicarbonate in blood were decreased accordingly. Clinical toxicity signs, including excess salivation, muscular tremors of legs, and excitability were observed with potassium doses greater than .58 g of potassium per kilogram body weight. Three of five calves given 1.73 g of potassium per kilogram, three of four calves given 2.31 g of potassium per kilogram, and one calf given 2.88 g of potassium per kilogram body weight died. With a small number of calves, oral sodium infusions increased plasma sodium in proportion to the dose, but plasma potassium remained relatively constant. Sodium infusions of 2.12 and 2.16 g of sodium per kilogram body weight were fatal.
Young male Holstein calves were fed either a control (.5% chloride) or a low-chloride (.038% chloride) practical diet for 7 wk. Both groups received low-chloride (.00038% chloride) well water. Feeding the low-chloride diet did not produce definite clinical symptoms of chloride deficiency. Neither body weight gains, feed intake, feed digestibility, nor body retention of chloride, sodium, potassium, or nitrogen were effected adversely. Although the chloride intake of the low-chloride calves was only one-sixteenth that of controls, body chloride retention was similar for the two groups. The similar retention of body chloride was due to effective homeostatic mechanisms in which urinary chloride excretion was reduced by 95% in the low-chloride calves. Low-chloride calves consumed more water and excreted more urine than control calves. Although the exact minimum chloride requirement for growth in calves was not established, .038% chloride was adequate for normal growth for the 7 wk.
A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).
The history, clinical signs, and clinical pathology in a mature Holstein cow were consistent with a diagnosis of intussusception, but the lesion found during exploratory laparotomy consisted of a penetrating wire in the anterior duodenum.
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Whole blood containing 59Fe-labeled erythrocytes (RBC) and unlabeled serum was transfused from a donor horse on 2 occasions into each of 6 recipient horses. Survival of transfused cells was monitored in the recipients as a function of time after transfusion by measuring RBC radioactivity in the recipients. After the 1st transfusion, RBC concentration of 59Fe remained at 60% to 100% of the transfused dose for 4 days, after which radioactivity values dropped to less than 10% of the dose by 6 days in 3 horses. In the 3 other horses, RBC radioactivity dropped immediately after transfusion, reaching minimal values in approximately 48 hours. After the 2nd transfusion, 1 horse retained 80% of the dose in circulating RBC for 4 days; 2 horses demonstrated a rapid loss of circulating radiolabeled RBC, reaching minimal values in 48 hours; and 2 horses demonstrated minimal radioactivity in the RBC mass even immediately after the transfusion. One horse died of anaphylactic shock during the 2nd transfusion. Erythrocyte compatibility tests, using the direct agglutination test, the antiglobulin test, and the hemolytic test, were not effective in predicting survival of transfused RBC.
Five horses of mixed breeding and 1 zebra with symmetric tetraparesis and ataxia were studied. There were 2 females and 4 males. Signs of illness were first noticed from birth to 12 months of age. Clinical and pathologic studies were performed when the animals were 4 to 24 months old. Two of the horses were related. All of the subjects had diffuse degenerative myeloencephalopathy. The degeneration was most pronounced in thoracic segments of the spinal cord. Ventral and dorsolateral funiculi were most severely affected. Axonal swelling and abnormal neuronal cell bodies were seen in the gray matter of the spinal cord and in some brain-stem nuclei. These changes were most prominent in the nuclei of the dorsal spinocerebellar tract. The cause was not determined.
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Cerebrospinal fluid (CSF) samples were collected from the atlanto-occipital (AO) and lumbosacral (LS) subarachnoid spaces of 24 horses and 21 ponies that had no clinical evidence of neurologic disease. Depth of needle insertion, pressures, refractive index, rapid reagent strip test (protein, glucose, blood, pH) results, cell counts, content of protein, glucose, sodium, potassium, chloride, calcium, phosphorus, urea nitrogen, and cholesterol, and activities of creatine phosphokinase, aspartate transaminase, lactic dehydrogenase, and alkaline phosphatase were determined. The resulting clinical reference values obtained were discussed in light of the published normal values for CSF from horses, other animals, and man. White cell counts in CSF were found to be from 0 to 6/microliters. Values for protein content were distributed between wider limits than previously reported values. The LS-AO difference is proposed as a criterion for clinical evaluation of CSF protein content. Ponies were found to have more protein in their CSF than did the horses, and CSF from the LS site contained more glucose than that from the AO site. The CSF electrolyte composition was similar to that of previous reports. Enzyme activities in equine CSF are reported for the 1st time.
Cecal dilatation in cattle is usually manifested by a syndrome of intestinal obstruction requiring surgical intervention. A patient is presented persistent dilatation of the cecum for ten months without evidence of impaired appetite or milk production. The initial clinical signs, progress of the case, and laboratory data are described.
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A postnatal cerebellar atazia of a type not previously reported in calves is described. Atazia was first noticed in affected animals when they were three to eight months of age, and was often accompanied by loss of the menace response in an animal which was not blind. The disorder was progressive. At postmortem cerebellar size was normal. Microscopic lesions consisted of primarily an apparent degeneration of cerebellar neurons without obvious evidence of inflammation. History, clinical signs, laboratory examination, gross pathology, histopathology, differential diagnosis, search for an etiologic agent and genetic histories are reported. It is concluded that this disorder may represent an hereditary cerebellar abiotrophy in Holstein cattle.
Polyuria in a herd of forty-five dairy cattle was the chief complaint in the first case. Polydipsia was the principle sign in a second case involving one dairy cow. Less conspicuous clinical findings included salt hunger, pica, weight loss and decreased milk production. Clinicopathologic investigation included monitoring the concentrations of sodium, potassium and chloiride in urine, parotid saliva and plasma. These analyses indicated a primary sodium deficiency which responded to sodium chloride ad libitum.
A case report of a young bull with persistent papillomatosis associated with immunodeficiency is presented. Humoral immune responses were normal but cell mediated immunity was deficient. The possible significance of the findings to pathogenesis and therapy of the disease is discussed.
A three-week-old Arabian filly was admitted to the Large Animal Hospital with a respiratory disorder and died despite symptomatic treatment. The necropsy lesions were suggestive of viral pneumonia. An equine adenovirus were isolated from nasal and pharyngeal swabs and from several tissues after death. Typical adenovirus virions were demonstrated by electron microscopy.