Septic pericarditis caused by a migrating grass awn in a cat.

Septic pericarditis and cardiac tamponade associated with migrating grass awn foreign bodies is reported rarely in companion animals. We report such a case in a previously healthy, 9-year-old, neutered female, indoor-outdoor, domestic long-hair cat who presented for acute tachypnea. Large volume pericardial effusion and pericardial tamponade was identified by thoracic-focused assessment with sonography. Following removal of 108 mL of purulent pericardial effusion by pericardiocentesis, the cat improved. Cytologic examination of pericardial fluid demonstrated septic, suppurative inflammation, Pasteurella sp. was cultured from pericardial effusion, and antibiotics were administered. Subsequent echocardiographic examination revealed large volume pericardial effusion, pericardial thickening, and a linear foreign body within the pericardial space. Whole-body computed tomography confirmed pericardial thickening, pericardial, and pleural effusion. A 16-mm long grass awn was identified within the pericardial space during thoracic exploratory surgery performed through a median sternotomy. Successful foreign body removal and subtotal pericardiectomy was accomplished. Histopathology of pericardial tissue disclosed chronic pericarditis with lymphoplasmacytic-to-pyogranulomatous inflammation, and transmural presence of grass awn foreign body. The cat responded to supportive therapy and was discharged 4 days postoperatively. When examined 3 weeks later, the cat appeared healthy with normal appetite. The cat remained healthy as of this writing, 487 days following surgery. To the author's knowledge, this is the first report in the cat of septic pericarditis and cardiac tamponade resulting from a migrating grass awn foreign body.

Investigation of iron status and markers of inflammation in anaemic and non-anaemic hospitalised cats.

OBJECTIVES: To measure iron parameters and markers of inflammation in anaemic cats presented for intensive care unit hospitalisation, and to compare these to cohorts of non-anaemic hospitalised cats and cats that develop hospital-acquired anaemia. METHODS: Blood samples were collected for measurement of iron panel and serum amyloid A in addition to routine investigation in cats admitted to the intensive care unit. Medical records were reviewed to determine how many of the Systemic Inflammatory Response Syndrome criteria were met and to assign Acute Patient Physiologic and Laboratory Evaluation scores as a measure of illness severity. RESULTS: Seventy-eight cats were enrolled. Anaemia was documented in 34·6% of cats on presentation and another 10·3% developed anaemia during hospitalisation. Compared with non-anaemic cats, animals that were anaemic on presentation had higher neutrophil and white blood cell counts, and longer hospitalisation. Iron status was consistent with anaemia of inflammation in most anaemic patients. Iron status, serum amyloid A concentration, and prevalence of systemic inflammatory response syndrome did not differ between anaemic and non-anaemic cohorts. All cause mortality was higher in anaemic cats. CLINICAL SIGNIFICANCE: Anaemia is common in cats hospitalised in the intensive care unit. Systemic inflammation is also common in these cats. Iron status in anaemic cats suggests that anaemia of inflammatory disease may be a significant contributor to anaemia in this patient population.

Purkinje cell dendritic arbors in chick embryos following chronic treatment with an N-methyl-D-aspartate receptor antagonist.

The normal development of Purkinje cell dendrites is dependent on afferent innervation. To investigate the role of neuronal activity in Purkinje cell dendritic development, chick embryos were chronically treated with a potent, selective, and systemically active competitive N-methyl-D-aspartate (NMDA) receptor antagonist, NPC 12626. The NMDA receptor was chosen as a target for pharmacological blockade because of the importance of the NMDA receptor in synaptic plasticity and stabilization in development. Chick embryos were given daily injections of NPC 12626 (25 to 100 mg/kg) from embryonic day 14 (E14) to E17. The initial injections of NPC 12626 dramatically blocked embryo movements, but activity levels partially recovered following subsequent injections. Embryo movements were reduced by 24% at the end of the experiment. Embryos were killed on E18, and their brains processed for Golgi-Cox staining. The morphology of Golgi-stained Purkinje cells in drug-treated embryos was similar to control embryos. Morphometric analysis showed, however, that chronic treatment with NPC 12626 resulted in a 19% reduction in Purkinje cell dendritic tree area and a 13% reduction in the number of dendritic branch points. The overall width and height of the drug-treated dendritic trees were not significantly different from controls, suggesting that NPC 12626 reduced Purkinje cell dendritic area by interfering with branch formation. The volume of the granule cell layer and the heights of the molecular and external granule cell layers was not reduced, suggesting that NPC 12626 treatment did not simply delay development. These results suggest that activation of the NMDA receptor may mediate the afferent-target interactions in the cerebellum that regulate the elaboration of Purkinje cell dendrites.

Topographic spinocerebellar mossy fiber projections are maintained in the lurcher mutant.

A variety of recent studies of cerebellar development have focused attention on the role of Purkinje cells as organizing elements for the topography of afferent fiber connectivity in the cerebellum. We have investigated the involvement of Purkinje and granule cells in the maintenance of topographic spinocerebellar mossy fiber projections by analyzing the distribution of spinocerebellar mossy fiber terminals in lurcher (+/Lc) mutant mice. Purkinje cells in the +/Lc mutant degenerate starting after the first week of postnatal development because of an intrinsic genetic defect. The loss of their Purkinje cell targets also results in the death of 90% of the granule cells. We examined the distribution of spinocerebellar mossy fiber terminals in the juvenile and adult +/Lc mutant to determine how the pattern of afferent projections is affected by the loss of Purkinje cells shortly after innervation of the cerebellum. Labeling of spinocerebellar mossy fiber terminals with WGA-HRP in the P38 and adult +/Lc mutant showed that, despite the loss of almost all Purkinje cells and 90% of the granule cells, spinocerebellar mossy fibers project to the appropriate folia and segregate into relatively normal parasagittal bands. While we cannot rule out the possibility that Purkinje cells may be involved in the initial establishment of topographic maps, our results indicate that Purkinje cells are not necessary for the maintenance of the normal spinocerebellar mossy fiber topographic map.