Neurological Manifestations of Niemann-Pick Disease Type C in Cats

Seven Domestic shorthair cats with a lysosomal storage disorder analogous to human Niemann-Pick disease type C, from a breeding colony were studied to characterize the neurological manifestations of this disorder. Affected cats were identified by means of liver biopsies at 4 to 6 weeks of age. Neurological examinations were performed at 2 week intervals from the onset of clinical signs. All cats displayed signs referrable to the cerebellum, with a subtle intention tremor noticed initially at 8 to 12 weeks of age; the disease was rapidly progressive. The tremor became more pronounced, menace response was lost, and severe dysmetria and ataxia developed. Three cats also had signs referrable to other areas of the central nervous system. Cats died or were euthanized between 12 and 43 weeks of age. Pathological findings included accumulation of substrate within neurons throughout the central nervous system, and axonal spheroid formation. The clinical and pathological findings in these cats are comparable to those in the human form of the disease.     

Acute and chronic hormone and metabolite changes in lambs fed the beta-agonist, cimaterol

The objective of this study was to determine if acute and chronic changes in circulating metabolic hormone and metabolite concentrations are associated with β-agonist-induced nutrient repartitioning in young growing lambs. Two groups of 12 Dorset and Dorset-Finn cross ram lambs weighing 36 or 33 kg live weight were assigned to 3- or 6-week treatment intervals, respectively, to achieve similar slaughter weights. Six lambs within each treatment interval were fed ad libitum a complete mixed high-concentrate diet containing either 0 or 10 ppm cimaterol. During the first 12 hr of cimaterol administration plasma somatotropin (ST), thyroxine (T₄), and triiodothyronine (T₃) concentrations were not altered by treatment, but plasma insulin, glucose, non-esterified fatty acids (NEFA) and glycerol concentrations were elevated 2 hr after ingestion. These acute responses suggest direct stimulation of glycogenolysis and lipolysis by cimaterol, which is characteristic of β-adrenergic alteration of carbohydrate and lipid metabolism. Chronic administration of cimaterol significantly decreased insulin concentrations by 36% and 52% at 3 and 6 weeks, respectively, while glucose concentrations remained unchanged. Serum IGF-I concentrations were not significantly altered by cimaterol. T₄ levels were reduced 22.1% after 3 weeks of cimaterol treatment. Although plasma NEFA concentrations were chronically elevated 56% to 65% in lambs fed cimaterol, plasma glycerol concentrations remained at baseline levels. The relative changes in plasma NEFA and glycerol concentrations are consistent with a decreased rate of lipogenesis, rather than an increase in lipolysis.     

The effects of bovine growth hormone and thyroxine on growth rate and carcass measurements in lambs

The effects of bovine growth hormone (GH) and thyroxine (T4) on growth and carcass characteristics were assessed in Dorset ram lambs. Lambs in four groups (n = 10/group) were treated for 30 d as follows: controls, 3.33 mg (6 IU) GH/d (s.c.); 5-mg T4 implant (s.c.) on d 1 and a 10-mg T4 implant 21 d later; GH + T4. Blood samples were collected at 3-d intervals for analysis of GH, T4, triiodothyronine, somatomedin-C and testosterone concentrations. Six lambs/group were slaughtered for carcass measurements and composition. Daily GH injections increased (P less than .005) baseline plasma GH levels 10-fold, whereas plasma T4 concentrations were increased 10% (P less than .10) by the implants. Somatomedin-C increased with time in all groups, but the increments from d 0 to d 30 were higher (P less than .05) with GH treatment. Average daily gain (mean = 352 g/d), feed consumption and feed to gain ratio were not affected (P greater than .1) by GH or T4 treatment in ram lambs. Hot carcass weight and dressing percentage were increased (P less than .05) by T4. Growth hormone increased carcass protein content (P less than .005) and muscle weights while reducing carcass fat (P less than .05). Carcass composition was not altered by T4 alone, and the T4 x GH interaction was not significant; however, the combination of T4 and GH resulted in greater muscle and protein weight than did either hormone alone or no hormone administration. There were no differences in bone length or in the metacarpal growth plate width among groups. The beneficial effects of GH on carcass composition were not further enhanced by administration of thyroxine.     

Proposed criteria for classification of acute myeloid leukemia in dogs and cats

Blood and bone marrow smears from 49 dogs and cats, believed to have myeloproliferative disorders (MPD), were examined by a panel of 10 clinical pathologists to develop proposals for classification of acute myeloid leukemia (AML) in these species. French-American-British (FAB) group and National Cancer Institute (NCI) workshop definitions and criteria developed for classification of AML in humans were adapted. Major modifications entailed revision of definitions of blast cells as applied to the dog and cat, broadening the scope of leukemia classification, and making provisions for differentiating erythremic myelosis and undifferentiated MPD. A consensus cytomorphologic diagnosis was reached in 39 (79.6%) cases comprising 26 of AML, 10 of myelodysplastic syndrome (MDS), and 3 of acute lymphoblastic leukemia (ALL). Diagnostic concordance for these diseases varied from 60 to 81% (mean 73.3 +/- 7.1%) and interobserver agreement ranged from 51.3 to 84.6% (mean 73.1 +/- 9.3%). Various subtypes of AML identified included Ml, M2, M4, M5a, M5b, and M6. Acute undifferentiated leukemia (AUL) was recognized as a specific entity. M3 was not encountered, but this subclass was retained as a diagnostic possibility. The designations M6Er and MDS-Er were introduced where the suffix "Er" indicated preponderance of erythroid component. Chief hematologic abnormalities included circulating blast cells in 98% of the cases, with 36.7% cases having >30% blast cells, and thrombocytopenia and anemia in approximately 86 to 88% of the cases. Bone marrow examination revealed panmyeloid dysplastic changes, particularly variable numbers of megaloblastoid rubriblasts and rubricytes in all AML subtypes and increased numbers of eosinophils in MDS. Cytochemical patterns of neutrophilic markers were evident in most cases of Ml and M2, while monocytic markers were primarily seen in M5a and M5b cases. It is proposed that well-prepared, Romanowsky-stained blood and bone marrow smears should be examined to determine blast cell types and percentages for cytomorphologic diagnosis of AML. Carefully selected areas of stained films presenting adequate cellular details should be used to count a minimum of 200 cells. In cases with borderline diagnosis, at least 500 cells should be counted. The identity of blast cells should be ascertained using appropriate cytochemical markers of neutrophilic, monocytic, and megakaryocytic differentiation. A blast cell count of > 30% in blood and/or bone marrow indicates AML or AUL, while a count of < 30% blasts in bone marrow suggests MDS, chronic myeloid leukemias, or even a leukemoid reaction. Myeloblasts, monoblasts, and megakaryoblasts comprise the blast cell count. The FAB approach with additional criteria should be used to distinguish AUL and various subtypes of AML (Ml to M7 and M6Er) and to differentiate MDS, MDS-ER, chronic myeloid leukemias, and leukemoid reaction. Bone marrow core biopsy and electron microscopy may be required to confirm the specific diagnosis. Immunophenotyping with lineage specific antibodies is in its infancy in veterinary medicine. Development of this technique is encouraged to establish an undisputed identity of blast cells. Validity of the proposed criteria needs to be substantiated in large prospective and retrospective studies. Similarly, clinical relevance of cytomorphologic, cytochemical, and immunophenotypic characterizations of AML in dogs and cats remains to be determined.     

A test for photorefractoriness in high‐producing stocks of laying pullets

1. Pullets of 2 high‐producing commercial stocks (both brown‐egg layers) were exposed to 5 different lighting patterns between 18 and 72 weeks to test the hypothesis that photoperiods used in commercial lighting programmes early in the laying year may be unnecessarily long and, by accelerating the development of photorefractoriness, may contribute to the decline in egg production observed after the initial peak. Two rooms of 288 pullets were allocated to each treatment.

2. The rate of lay observed with a Step‐Up treatment which gave increases in photoperiod from 8L:16D at 18 weeks to 15L:9D at 27 weeks of age was not significantly different from that of treatments which held the birds on 11L:13D during peak egg production but gave increments up to 15L:9D later in the laying year.

3. A control group maintained on 11L:13D from 20 to 72 weeks laid 295 eggs per bird housed and a further group held on 8L:16D from 0 to 72 weeks laid 284 eggs per bird. These yields were lower than the Step‐Up treatment (299 eggs) but show the potential of modern hybrid stocks to lay prolifically even without light stimulation.

4. It is concluded that the stocks tested in this experiment showed no advantage when given lighting programmes in the first laying year which were designed to minimise the adverse effects of photorefractoriness.