PubMed Health⌕ Search

Biomedical subjects

M M Walser

Publications and source records attributed to M M Walser.

32 records · Page 2Linked to original sources

Toxicity of gentamicin in red-tailed hawks.

Gentamicin sulfate at dosage levels of 10 and 20 mg/kg of body weight was administered twice daily IV to red-tailed hawks. Clinical signs, water consumption, and changes in blood chemical values were monitored. Tissues were examined grossly and ultrastructurally, using light and electron microscopy. Clinical signs of weakness and apnea were attributed to gentamicin-induced neuromuscular blockade in the 20-mg/kg group. Serum values of aspartate transaminase, alanine transaminase, cholesterol, inorganic phosphorus, total protein, albumin, and uric acid increased in some birds. There was a decrease in periodic acid-Schiff staining of proximal tubular brush borders. Increased numbers of cytoplasmic lysosomes, many of which contained myelin figures, in renal epithelial cells were seen at the ultrastructural level. All birds given 20 mg/kg died. Both dosage levels were considered toxic in red-tailed hawks.

Animals↗

Fusarium-induced osteochondrosis (tibial dyschondroplasia) in chickens.

Broiler chickens were started and maintained on rations containing 2%, 5%, and 10% grain contaminated with Fusarium roseum. There was mortality of 75% and 100%, respectively, in chicks fed 5% and 10% levels, and osteochondrosis was present in chicks which died at 12 to 17 days of age. Chicks on 2% or 3% F. roseum-contaminated grain survived the experimental period and osteochondrosis was well-developed in the proximal tibias of 85 or 99% of these chicks. The number of chondroclasts was reduced markedly in the affected bones. Defective chondroclasis may play a role in the pathogenesis of osteochondrosis associated with F. roseum.

Animals↗

Toxic effects of repeated ethanol intubations to chicks.

Dosages of 95% ethanol (0, .5, or 1 ml) with variable quantities of water were administered to mixed sex chicks (263 g initial weight) on each of 7 consecutive days. The 1 ml dosage of ethanol significantly reduced body weight gains and feed consumption and increased liver weight per 100 g of body weight. Gross crop lesions (accumulation of exudates and hemorrhage) were observed for both the .5 and 1 ml dosage level of ethanol. For birds given the .5 ml ethanol dosage, dilution with water tended to reduce the severity of crop lesions but not for birds given 1 ml ethanol. All levels of ethanol produced mild ataxia within 5 to 10 min of dosage. Mild or moderate hepatocellular fatty change was present in livers from 5 to 6 birds given 1 ml ethanol. Crop exudates were composed of necrotic cells, fibrin and bacteria. Crop walls of birds given 1 ml of undiluted ethanol were ulcerated and inflamed. Areas within the crop wall were hemorrhagic, edematous, and infiltrated by heterophils and mononuclear cells.

Animals↗

Evaluation of niridazole as a suppressant of cellular immunity in chickens.

Niridazole was administered by gavage to 5-week-old chickens at dosage levels of 50, 100, and 200 mg/kg of body weight. The 2 larger dosage levels were toxic and resulted in the death of many of the recipients. The 50 mg/kg dosage level was not lethal, but depressed weight gain. Cellular immune functions were measured by responses of lymphocytes in whole blood to T-cell mitogens and by delayed hypersensitivity reactions to tuberculin. Blastogenic responses to phytohemagglutinin and concanavalin A were reduced in niridazole-treated chickens with responses of controls. Wattle tests measuring delayed hypersensitivity were positive only in control chickens; reactions in niridazole-treated chickens did not differ from nonimmunized controls.

Animals↗

Dose response, prevention, and treatment of a transplantable lymphoid tumor.

Transplantable lymphoid tumor (TLT) cells in doses ranging from 10(2.43) to 10(6.80) were transplanted into 3-week-old chicks. A total of 199 chicks in 31 dosage groups was included in this 2-year study. Overall mortality was nearly 100% and analysis of the results revealed no significant differences in mortality among the groups. A significant (P less than 0.001) linear relationship existed between log10 of the TLT cell dose and mean survival time. Serum obtained from chickens which survived TLT growth, regression, and challenge inoculation was administered to chicks 4, 7, or 11 days before TLT induction. Of the chickens in each of these 3 groups, 80 to 100% survived compared with 0 to 20% in those given control serum. In chicks with actively growing TLT that were treated with 2 injections of plasma from TLT-resistant chickens, mean survival time was lengthened and survival was increased by 36%. Lymphocytes from resistant chickens or plasma od and survival was increased by 36%. Lymphocytes from resistant chickens or plasma or lymphocytes from control chickens did not affect survival time or percentage of survival. In the present study, results demonstrated a similarity to the TLT model studied 30 years ago and established the usefulness of this model in the study of serum immunotherapy.

Animals↗

In vitro characterization of field isolants of Pasteurella multocida from Georgia turkeys.

Field isolants of Pasteurella multocida from fowl cholera outbreaks in Georgia turkeys were characterized by three sets of criteria: differential biochemical reactions, in vitro drug sensitivity, and serology. Of the 30 isolants studied, 28 exhibited identical biochemical patterns. These were similar to previously described patterns for turkey isolants of P. multocida. The two exceptions were isolants recovered from the same farm at different times. They differed only in ability to ferment arabinose. The isolants were generally sensitive to broad-spectrum antibiotics in vitro. The majority were also sensitive to the sulfonamides tested. Variation was sufficient, however, to warrant recommending in vitro sensitivity testing as a guide to selection of the proper therapeutic regimen in individual cases. Of the 30 isolants tested, 57% were of Heddleston's serotype 3, 3% were of his type 4, and 40% precipitated with antisera against both types 3 and 4. The large proportion of cross-reactors is unique to Georgia isolants. The biochemical patterns, drug sensitivities, and serological types had no apparent relationship to each other.

Animals↗

Effect of dietary selenium on the development of Fusarium-induced tibial dyschondroplasia in broiler chickens.

A trial was conducted to determine the effects of dietary level of selenium on the pathogenesis of Fusarium-induced tibial dyschondroplasia (FITD) in broiler chicks, and to assess the applicability of FITD as an animal model of Kashin-Beck disease of humans. Day-old female broilers were fed diets that were deficient in selenium (0.02 ppm Se), adequate in selenium (0.15 ppm Se), or generous in selenium (0.50 ppm Se). TDP-1, the toxic component of the fungus, was administered to 15 of 26 chicks in each dietary group starting at 1 week of age and continuing until the chicks were killed at 24-30 days of age. Plasma selenium levels and hepatic glutathione peroxidase activity were significantly lower in the selenium-deficient group than in other dietary groups; these parameters were not affected by treatment with TDP-1. The mortality rate of the TDP-1-treated selenium-generous group was significantly less than that in the other TDP-1-treated groups, but there were no differences in the incidence, severity, or character of the FITD lesions among the groups. Thus, the interaction of selenium and TDP-1 did not include an effect on FITD.

Amino Acids↗

Acid phosphatase activity of chondroclasts from Fusarium-induced tibial dyschondroplastic cartilage.

Tibial dyschondroplasia was induced in broiler chickens by oral administration of fusarochromanone, the toxic component of Fusarium equiseti. In two experiments, the activity of acid phosphatase in chondroclasts was assessed histochemically. Chicks were examined at 7, 14, 21, and 28 days of treatment in Expt. 1 and at 2, 4, and 6 days of treatment in Expt. 2. The staining for acid phosphatase was consistently lower in fusarochromanone-treated chicks after 2 days of treatment than in age-matched controls, and the onset of this difference corresponded to the onset of lesions. However, the decrease in acid phosphatase staining intensity was significant only at day 21 in Expt. 1 and at day 6 in Expt. 2. The deficiency of acid phosphatase in chondroclasts was judged to be of insufficient magnitude to account for the accumulation of growth plate cartilage that characterizes tibial dyschondroplasia.

Acid Phosphatase↗

Histologic features of transplantable lymphoid tumor (Olson) during growth and regression induced by serum therapy.

Susceptible 3-week-old chicks were inoculated with cells of an avian transplantable lymphoid tumor (TLT) and then treated with serum from immune chickens, serum from control chickens, or balanced salt solution. Progressive tumor growth was observed in chickens of all 3 treatment groups. Tumor growth was followed by regression only in chicks treated with immune serum. Regression was characterized by necrosis of tumor cells, muscle regeneration, and lymphocyte and plasma cell infiltration.

Animals↗

Field rickets in turkey poults: biochemical findings.

Two clinical cases of field rickets and one of nutritional rickets in turkey poults were studied. Plasma levels of calcium, phosphorus, alkaline phosphatase, and vitamin D metabolites were determined. Concentrations of calcium, phosphorus, and alkaline phosphatase in affected poults were typical of nutritional rickets. The mean plasma calcium concentration in rachitic poults was not significantly different from that in controls. Mean values for plasma phosphorus were 1.5 to 2.4 mg/dl lower in the rachitic poults, and values for alkaline phosphatase activity were 1.3-1.7 times greater. In assays of vitamin D metabolites, mean 24, 25 dihydroxyvitamin D3 values were consistently lower in rachitic poults.

24,25-Dihydroxyvitamin D 3↗

Osseous development and tibial dyschondroplasia in five lines of turkeys.

Tibiotarsi and femurs from five genetic lines of turkeys from 8 to 39 weeks of age were examined to define the characteristics of normal bones. Bone lengths and body weights are presented. Tibial dyschondroplasia (TD) frequently was detected on gross examination and by high-detail radiography. The incidence of TD peaked at 12 weeks of age, when 79% of the toms were affected. This incidence rate dropped until the age of closure of the proximal tibial physis (22 to 24 weeks in toms) but remained 5 to 15%. Deformities of the tibiotarsi were frequently associated with TD in older toms. The incidence of TD and tibiotarsal deformities was highest in toms of the heaviest line.

Age Factors↗

"Field rickets" in turkey poults: field observations and pathological, radiological, and serological findings.

Two field cases of field rickets in turkey poults were studied. The primary observation was lameness, and the sole necropsy finding of significance was hypomineralization of bone. This finding was confirmed radiographically; thin cortices and wide growth plates were noted. Microscopically, there was failure of osteoid mineralization, failure of orderly progression from cartilage to bone in the growth plate, the formation of bony trabeculae perpendicular to the long axis of the bone, and fibroplasia in marrow spaces. On a routine serological screen for mycoplasma and several viruses, there were no differences between affected and normal poults from the same flock.

Animals↗

Effects of aflatoxin B1 on chicken chondrocytes in culture.

In vitro effects of aflatoxin B1 on DNA and proteoglycan synthesis were assessed by measuring tritiated thymidine and radiosulfate incorporation by chicken chondrocyte cultures. Chondrocytes were harvested from the growth-plate cartilage of a 35-day-old chicken, cultured in triplicate, and treated with 0, 1, 5, 10, or 25 micrograms aflatoxin B1/ml of culture medium. The cultures were then spiked separately with [3H]thymidine or [35S]sulfate. After the cells, matrix, and medium were harvested, radioactivity was measured by a scintillation counter. Aflatoxin B1 resulted in a dose-dependent inhibition of DNA synthesis, as measured by tritiated thymidine incorporation by chicken chondrocytes: 54.6%, 30.9%, 25.9%, and 5.9% of control in cultures treated with 1, 5, 10, and 25 micrograms aflatoxin B1/ml of culture medium, respectively (P < 0.05). Sulfated proteoglycan synthesis, as measured by radiosulfate incorporation in chondrocyte cultures, was decreased in the media and intercellular matrix by all aflatoxin B1 levels. Compared with controls, 21% less (P < 0.05) radiosulfate was incorporated into non-matrix macromolecules of the medium fraction from chondrocytes exposed to 1 microgram aflatoxin B1/ml. However, 5 micrograms aflatoxin B1/ml was necessary to produce a significant decrease in radiosulfate incorporation in proteoglycans of intercellular matrix (34% less than controls). The ratios of the means of radiosulfate incorporation into intercellular macromolecules to the means of tritiated thymidine incorporation indicated that aflatoxin B1 inhibited DNA synthesis more than proteoglycan synthesis.

Aflatoxin B1↗

An antiviral effect of nitric oxide: inhibition of reovirus replication.

We have previously shown that macrophages from chickens infected with avian reovirus are primed to produce nitric oxide (NO) in response to T cell cytokines and bacterial lipopolysaccharide (LPS). We now show that NO exerts potent antireovirus effects. Reovirus replication was substantially reduced in a chicken macrophage cell line, HD11, induced to make NO by stimulation with LPS or conditioned medium from concanavalin A-stimulated spleen cells. The use of a competitive inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine, reduced the antiviral effect of LPS-stimulated HD11 cells. Cytostatic effects were concurrent with the observed antiviral effects of NO. Among these cytostatic effects were reduction in DNA synthesis, protein synthesis, and mitochondrial metabolism. These results indicated that a potential consequence of macrophage priming following virus infection is the protection of cells against virus-induced replication and cytopathic effects, and this protection may be mediated by the cytostatic effects of NO on the host cell.

Animals↗