Failed epidural and the new epidural fixation device.
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Biomedical subjects
Publications and source records attributed to J E Bellamy.
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The complexity and uncertainty of diagnostic information makes the diagnostic process difficult to learn, teach, and practice. Fuzzy logic methods, used successfully with complex industrial control problems, may be appropriate to model the range of uncertainties found in medical diagnostic information. A fuzzy systems model for use with diagnostic and other medical decisions is described. Combining a state space view of an animal in which each dimension of the space represents a variable of the animal with a fuzzy sets representation of the variables and states of the animal leads to a fuzzy systems model, which can be used to successfully diagnose disease. Partitioning the multidimensional state space of the animal into healthy and specific disease regions provides a diagnostic space for evaluating the health of the animal. When an input vector representing the variables of a sick animal is entered into the system, the model can provide a diagnosis and, potentially, a prognosis for that animal. The model can be implemented on a desktop computer for convenient use, and it provides a helpful geometric interpretation of the concepts of "diagnosis" and "prognosis" for teaching diagnostic reasoning. The fuzzy systems approach has advantages that are unavailable in other methods. The capability of fuzzy systems to act as universal approximators allows them to accommodate complex, nonlinear, imprecise, and even conflicting relationships to provide accurate knowledge representation. With these advantages over standard rule-based methods of modeling the medical diagnostic process, fuzzy expert systems have broad potential for use in medicine and warrant further study to determine their application and possible limitations.
A computer-based fuzzy systems approach to diagnosis was compared with a standard rule-based approach for ability to diagnose 1 or more of 14 diseases in postpartum cows. A comparison between the 2 systems, using the same 12 input variables (clinical signs and laboratory measurements), resulted in 93% diagnostic agreement. Much of the study compared a fuzzy diagnostic system that had 12 input variables with a standard system that had 17 input variables. The results indicated that the fuzzy diagnostic system was more efficient to design (fewer rules), that the fuzzy system often provided a more accurate diagnosis, and that selection of input variables is critically important to diagnostic accuracy for any computer-based diagnostic system. The apparent advantages of fuzzy logic-based decision systems over standard rule-based methods of modeling the medical diagnostic process warrant continued study to determine limitations and other possible applications.
This study was carried out to determine the diagnostic usefulness of postmortem eyefluid analysis in estimating antemortem concentrations of serochemical constituents. A total of 31 cattle, 18 dogs and 22 cats were selected from routine elective euthanasia submissions to a diagnostic laboratory. For all cases, a biochemical profile, including determinations for electrolytes, glucose, urea, creatinine, enzymes, cholesterol, bilirubin, protein and osmolality was performed on antemortem serum, and postmortem aqueous and vitreous humors at 0 and 24 h incubation periods. The association between serum and postmortem eyefluid chemistry values was examined using simple linear regression. A strong correlation between serum and postmortem eyefluid urea and creatinine concentrations was demonstrated in the three species examined over a 24 h postmortem interval. We concluded that an accurate estimate of antemortem serum urea or creatinine can be made from the analysis of aqueous or vitreous fluid at necropsy. An estimation of antemortem serum electrolytes (including calcium in cattle) cannot be made with a high degree of accuracy due to the amount of variability in the relationship between serum and eyefluid electrolyte values. For large molecules such as proteins, enzymes, cholesterol and bilirubin there was very poor correlation between serum and eyefluid values.
Mouse inoculation was used to test for the presence of a toxin in the serum, cerebrospinal fluid, and intestinal contents collected from cases of bovine enteric coccidiosis, with and without neurological signs, and from control calves. Intravenous inoculation of mice with 10 mL/kg of serum from calves showing nervous signs caused effects significantly different from those caused by the inoculation of serum from calves not showing nervous signs and from control calves. The effect was particularly evident in female mice. At this dosage severe neurological signs such as loss of righting reflex, seizures and death occurred only with serum from calves with "nervous coccidiosis". The results suggest that serum from the calves with neurological signs contains a neurotoxin. This toxin appears to be highly labile. It was not present in the cerebrospinal fluid at levels comparable to those in the serum. The significance of this labile neurotoxin with respect to the pathogenesis of the neurological signs associated with bovine enteric coccidiosis is unknown.
Reported are the results of preliminary attempts to characterize the molecular weight, heat sensitivity and other features of a labile neurotoxin identified in the serum of calves exhibiting neurological signs in association with coccidial enteritis. The labile neurotoxin activity is heat labile (60 degrees C for 30 min) and is lost upon exposure to acidic pH (5.5) and cysteine (1.75 g/100 mL serum). Activity can be recovered from the precipitate of a 30% wt/vol solution of (NH4)2SO4 in serum. Ultrafiltration trials suggest that labile neurotoxin activity may be linked to a molecule of over 300,000 MW.
Various hypotheses have been proposed for the pathogenesis of the neurological signs associated with bovine enteric coccidiosis. We undertook a prospective study of cases of bovine enteric coccidiosis with and without nervous signs to test the validity of these hypotheses and explore other possible pathophysiological mechanisms. Clinical, pathological and toxicological data from 12 calves with, and 15 calves without, neurological signs were compared. Calves with neurological signs had a lower liver Cu concentration (p less than 0.01) and a higher plasma glucose concentration (p less than 0.05) than did calves without neurological signs. Hyperglycemia and Cu deficiency may increase the susceptibility to central nervous system damage, but are not likely to account for the onset of neurological signs in calves with enteric coccidiosis. The results of the study suggest that the following are not involved in the pathogenesis of "nervous coccidiosis": disturbance of serum Na, K, Ca, P, or Mg concentration, vitamin A deficiency, thiamine deficiency, anemia, lead intoxication, uremia, Haemophilus somnus meningoencephalitis, severity of coccidial infection, gross alterations in intestinal bacterial flora and hepatopathy.
Glucocorticoid treatment in dogs is known to cause hepatocellular swelling due to accumulation of cytoplasmic compounds which variably have been identified histochemically as fat, glycogen, or water. In the present study changes in dog liver, after treatment for 15 days with two different doses of oral or intramuscular prednisone, were examined using histological, histochemical, and ultrastructural techniques as well as quantitative chemical analysis. Thirty mongrel dogs were divided into two control groups and three treatment groups of six dogs each. Dogs which received prednisone orally at 1.2 mg/kg body weight/day, or 4 mg/kg body weight/day, respectively, or received intramuscular prednisone injections of 4 mg/kg body weight/day had hepatomegaly due primarily to hepatocellular accumulation of glycogen. Compared to controls, no changes in the hepatic water concentration were observed, whereas the relative amounts of liver fat were decreased slightly and those of protein were decreased markedly. Hepatocellular glycogen could be demonstrated histochemically in tissues fixed in absolute alcohol, but not in tissues treated with aqueous fixative, such as 10% buffered formalin or Bouin's solution. Glycogen deposition occurred predominantly in the midzone of hepatic acini. Affected hepatocytes varied in size and shape. The most severely affected cells were enlarged five to ten fold with glycogen occupying most of the cytoplasmic space restricting the mitochondria, endoplasmic reticulum, and other organelles to a narrow zone around the cell periphery and the nucleus. It was concluded that treatment with prednisone causes hepatomegaly due to glycogenosis in the dog.
In order to test the hypothesis that treatment with glucocorticoids causes pancreatitis in dogs, 18 mongrel dogs were divided into three groups of six individuals, each group receiving prednisone at different doses orally or intramuscularly for two weeks. Two groups consisting of six dogs each served as controls. Treatment for two weeks with oral prednisone at 1.2 mg/kg body weight or at 4 mg/kg body weight daily decreased the serum amylase activities, but increased the serum lipase activities. Postmortem examinations revealed microscopic evidence of mild pancreatitis in only one dog given prednisone, that clinically appeared normal. It was concluded that daily doses of 4 mg prednisone/kg body weight or less given orally or intramuscularly for two weeks do not cause pancreatitis in dogs.
Enterotoxigenic colibacillosis was experimentally produced in four colostrum-deprived calves given 10(10) Escherichia coli strain 210 (serotype 09+:K30+:K99-:F41-:H-) orally and the histopathological changes compared to those seen in colostrum-fed calves infected in an earlier study with strain B44 (serotype 09+:K30+:K99+:F41+:H-). Escherichia coli strain 210 caused diarrhea, atrophic villi with cuboidal epithelium, and focal accumulations of a few neutrophils in the dome villi above Peyer's patches but neither the clinical nor the histopathological changes were as pronounced as with strain B44. The extent and distribution of adherence to the mucosal surface differed between the two strains. Strain B44 adhered as a continuous layer over most of the absorptive epithelial surface of both the jejunum and ileum. Adherence of strain 210 was restricted to the ileum and the bacteria often adhered focally in "clumps" rather than as a continuous layer, especially on the distal half of the villous surface.
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Electrolyte and urea levels of vitreous humor collected from bovine eyes at various times postmortem, were compared with serum levels in the same animals. Provided the vitreous humor was filtered immediately after collection, measured levels of total calcium (Ca), potassium ions (K+), sodium ions (Na+) and urea nitrogen were very consistent. For 24 hours postmortem the concentrations of Ca, Na+ and urea nitrogen remained stable, while K+ increased to approximately 55% more than the immediate postmortem level. A small study using anesthetized dogs indicated that urea nitrogen levels of vitreous humor take several hours to equilibrate with elevated blood levels. Analysis of vitreous humor may be a useful adjunct to diagnosis in cases where antemortem clinical chemistry is absent or inadequate.
Intestinal loops, ligated in colostrum-deprived calves were used to compare the virulence of four isolates of bovine rotavirus. Histopathological studies were carried out on infected and control loops and measurements of villous length, crypt depth, villus:crypt ratio and crypt mitotic index were recorded. Pathological changes associated with the rotaviruses included villous atrophy, flattening of absorptive epithelium and reduced villus:crypt ratios. The changes were confined to infected intestinal loops in which the presence of virus was demonstrated by specific immunofluorescence. Consistent differences in the measured histopathological changes suggested differences in virulence among the rotavirus isolates tested. The least virulent rotavirus isolate had a polypeptide electrophoretic pattern that differed from the other three more virulent isolates.
The microhematocrit heat-precipitation methods of Millar et al (1971) and Schalm et al (1975) were compared with the reference clottable protein method of Ratnoff and Menzie (1951) in the measurement of plasma fibrinogen concentration in horses. The millar et al method was more precise and accurate and showed better positive correlation with the reference method than did the Schalm et al method. There was no significant difference in the plasma fibrinogen concentration between healthy Thoroughbreds and healthy horses of other breeds. Horses with bacterial pneumonia and abscesses had significantly greater plasma fibrinogen values than did those with colic, fractures, and nonsuppurative wounds. The Millar et al method was recommended as a simple, relatively accurate procedure for the determination of plasma fibrinogen that might be used as an additional diagnostic and prognostic indicator in the laboratory investigation of diseases in the horse.
Changes in hematopoietic and lymphoid tissues of young Swiss mice fed a balanced semipurified diet containing T-2 toxin (20 ppm) were examined after one, two, three, four or six weeks. During the first three weeks of exposure of T-2 toxin, lymphoid tissues, bone marrow and splenic red pulp became hypoplastic, resulting in anemia, lymphopenia and eosinopenia. Subsequently, during continued exposure to T-2 toxin, hematopoietic cells regenerated in bone marrow and splenic red pulp and became hyperplastic by six weeks. Granulopoiesis and thrombopoiesis resumed in advance of erythropoiesis. All lymphoid tissues remained atrophic throughout the six week trial. Mice exposed to T-2 toxin also developed perioral dermatitis and hyperkeratosis with ulceration of the mucosa of the esophageal region of the stomach. These results indicated that young mice were susceptible to both the irritant and the hematopoietic-suppressive toxic effects of dietary T-2 toxin. However, supression of hematopoiesis was transient and did not lead to hematopoietic failure.
Mice immunized with infections of 500, 5,000, or 20,000 oocysts of E. falciformis var. pragensis were reinfected with 20,000 and 100,000 oocysts at 20 and 38 days, respectively, after the initial infection. After the first challenge infection, none of the immunized mice showed clinical signs of coccidiosis; a few mice passed very low numbers of oocysts, and oocyst discharge seemed to correlate negatively with immunizing dose. None of the mice immunized twice passed oocysts after challenge. Mice immunized with three infections were completely immune to challenge for 4 months. The effect of the immune response on the life cycle of the coccidium was determined by histological examination of the intestines of immune and nonimmune mice infected with the parasite. In both the immune and nonimmune groups, sporozoites penetrated absorptive epithelial cells and migrated to crypt epithelial cells during the first 6 to 24 h postinfection. At 48 to 72 h postinfection, the sporozoites developed into mature first-generation schizonts in the nonimmune mice, whereas the developing first-generation schizonts degenerated within the crypt epithelial cells of the immune mice. In nonimmune mice, third-generation merozoites, inoculated intracecally, developed into mature fourth-generation schizonts, whereas in immune mice the developing fourth-generation schizonts degenerated before maturing. The possibility that a cellmediated immune mechanism is responsible for the arrest in schizogony is discussed.