Dominguita Lühers Graça

Causas de morte e razões para eutanásia de cães da Mesorregião do Centro Ocidental Rio-Grandense (1965-2004)

The main objective of this study was to investigate the prevalence of diseases culminating with death or motivating euthanasia of dogs from the midland region of the Midwest of Rio Grande do Sul State, Brazil. The necropsy files of the Laboratorio de Patologia Veterinaria (LPV) of the Universidade Federal de Santa Maria (UFSM) were accessed and necropsy protocols of dogs necropsied between January 1965 and December 2004 were reviewed. During this period 4,844 reports of canine necropsies were filed at the LPV-UFSM. The case distribution in relation to the disease categories diagnosed was as follows: infectious and parasitic diseases (1,693 [35.0%]); neoplasms (378 [7.8%]); disorders caused by physical agents (369 [7.6%]); degenerative diseases (342 [7.1%]); poisonings and toxinfections (112 [2.3%]); euthanasia due to convenience (101 [2.1%]); metabolic and endocrinological diseases (97 [2.0%]); iatrogenic disorders (83 [1.7%]); developmental disorders (25 [0.5%]); immune mediate diseases (10 [0.2%]); and nutritional disorders (6 [0.1%]). Other disorders, including multifactorial or idiopathic diseases contributed 80 (1.6%) cases. In 1,548 (32.0%) out of the 4,844 cases it was not possible to establish either cause of death or reason for euthanasia. Infectious and parasitic diseases (mainly canine distemper, parvoviral enteritis and intestinal parasitism), neoplasia (mainly mammary neoplasms and lymphoma), disorders caused by physical agents (mainly accidents caused by automotive vehicles) and degenerative diseases (mainly chronic renal failure, cirrhosis, and congestive heart failure) were the main disease categories causing death or motivating euthanasia in dogs of this midland region. However, when cases were evaluated in relation with the age of the dog, the disease prevalence differed. The main causes of death in puppies were infectious and parasitic disease (mainly parvoviral enteritis, canine distemper, and intestinal parasitism). In adult dogs the most important causes of death were canine distemper, neoplasia and trauma. In age dogs, approximately half of the deaths could be attributed to neoplasia and degenerative disease.

Cinomose: achados epidemiológicos de 250 casos

A review of the number of dogs submitted for necropsy at the Department of Veterinary Pathology of the Federal University of Santa Maria, RS, between 1985-1997 has shown that 11.7% (250/2136) had lesions and inclusion bodies characteristic of infection by canine distemper virus (CDV). Most of these cases occurred during the winter months in dogs that were less than 1.5 year old, which were submitted by residents from the city of Santa Maria. Canine distemper is considered endemic in this city. Significant differences in susceptibility were not observed between males and females. Mongrel dogs were super-represented, but dolichocephalic breeds were more affected than brachycephalic ones. Distemper encephalopathy with typical CDV inclusion bodies, especially in astrocytes, was the main lesion and occurred in 82% of these cases. Eosinophilic inclusion bodies characteristic of canine distemper were also observed in epithelial cells of the urinary bladder (15%), lung (6%), stomach (3%), kidney (1%), and tonsil (0.5%).

Pre-treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

The ethidium bromide (EB) demyelinating model was associated with vitamin E (Vit E) and ebselen (Ebs) treatment to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and erythrocytes. Rats were divided into seven groups: I—Control (saline), II—(canola); III—(Ebs), IV—(Vit E); V—(EB); VI—(EB + Ebs) and VII—(EB + Vit E). At 3 days after the EB injection, AChE activity in the CC and HC was significantly reduced in groups III, IV, V, VI and VII (p < 0.05) and in the ST it was reduced in groups III and V (p < 0.05) when compared to the control group. At 21 days after the EB injection, AChE activity in the CC was significantly reduced in groups III, IV and V, while in groups VI and VII a significant increase was observed when compared to the control group. In the HC and ST, AChE activity was significantly reduced in groups V, VI and VII when compared to the control group (p < 0.05). In the erythrocytes, at 3 days after the EB injection, AChE activity was significantly reduced in groups III, IV, V, VI and VII and at 21 days there was a significant reduction only in groups VI and VII (p < 0.05) when compared to the control group. In conclusion, this study demonstrated that Ebs and Vit E interfere with the cholinergic neurotransmission by altering AChE activity in the different brain regions and in the erythrocytes. Furthermore, treatment with Vit E and Ebs protected against the demyelination lesion caused by EB. In this context, we can suggest that ebselen and Vit E should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with demyelinating events.

Aspectos clinicopatológicos de 620 casos neurológicos de cinomose em cães: Clinicopathological features in 620 neurological cases of canine distemper

The files of 5,361 necropsies performed in dogs in the Veterinary Pathology Laboratory of the Federal University of Santa Maria during 1965-2006 were reviewed in search of cases of canine distemper. Six hundred and eighty three cases (12.7%) of the disease were found, 620 of which had neurological signs. From those 620, the following data on each case were retrieved: age, clinical signs, histopathology and concomitance or not of another disease. Age groups were classified as puppies (up to 1 year of age), adults (from 1 to 9 years) and aged (from 10 years on). In 565 out of the 620 (91.1%) neurological cases of canine distemper, histopathological brain changes were observed and in 554 of those 565 the age was registered in the files with following age group distribution: 45.9% of puppies, 51.4% of adults, and 2.7% of aged dogs. Neurological clinical signs encompassed a large spectrum of motor, postural and behavioral disturbances which could occur together or individually. Most frequent clinical signs were myoclonus (38.4%), motor incoordination (25.0%), seizures (18.5%), and paraplegia (13.4%). In 98.4% of the 565 dogs with histopathological changes in the brain demyelination, non-suppurative encephalitis or a combination of these two were found. Intranuclear eosinophilic inclusion bodies were observed in different brain cells of 343 of the 565 dogs with histopathological changes. In 170 (49.6%) the cellular type bearing the inclusions was not mentioned in the file and in the remaining cases the inclusions were seen in astrocytes (94.8% of the cases), neurons (3.5%), oligodendrocytes (1.1%), and ependyma cells (0.6%). Taking in consideration the type of lesions and the age groups, cases with combined demyelination and non-suppurative encephalitis occurred in 40.0% of the puppies, 51.2% of the adult dogs and 72.7% of the aged dogs. Demyelination alone occurred in 48.4% of the puppies, 41.3% of the adults and in 35.7% of the aged dogs. Non-suppurative encephalitis alone occurred 11.6% of the puppies, 7.5% of the adults and in 7.1% of the aged dogs.

Behaviour of oligodendrocytes and Schwann cells in an experimental model of toxic demyelination of the central nervous system

Oligodendrocytes and Schwann cells are engaged in myelin production, maintenance and repairing respectively in the central nervous system (CNS) and the peripheral nervous system (PNS). Whereas oligodendrocytes act only within the CNS, Schwann cells are able to invade the CNS in order to make new myelin sheaths around demyelinated axons. Both cells have some limitations in their activities, i.e. oligodendrocytes are post-mitotic cells and Schwann cells only get into the CNS in the absence of astrocytes. Ethidium bromide (EB) is a gliotoxic chemical that when injected locally within the CNS, induce demyelination. In the EB model of demyelination, glial cells are destroyed early after intoxication and Schwann cells are free to approach the naked central axons. In normal Wistar rats, regeneration of lost myelin sheaths can be achieved as early as thirteen days after intoxication; in Wistar rats immunosuppressed with cyclophosphamide the process is delayed and in rats administered cyclosporine it may be accelerated. Aiming the enlightening of those complex processes, all events concerning the myelinating cells in an experimental model are herein presented and discussed.Oligodendrocitos e celulas de Schwann realizam a producao e manutencao das bainhas de mielina, respectivamente no sistema nervoso central (SNC) e periferico (SNP). As celulas de Schwann, a diferenca dos oligodendrocitos, sao capazes de invadir o SNC para remielinizar axonios desmielinizados, sempre que os astrocitos tenham sido destruidos. O brometo de etidio e uma droga gliotoxica usada para induzir desmielinizacao com o desaparecimento precoce de astrocitos, de modo que as celulas de Schwann tem liberdade para invadir o SNC. Em ratos Wistar normais, a remielinizacao e detectada treze dias apos desmielinizacao; em ratos Wistar imunossuprimidos com ciclofosfamida a reparacao do tecido e tardia, enquanto que em animais tratados com ciclosporina ela e acelerada. O objetivo do artigo e discutir todas as etapas do processo de destruicao e reparacao da mielina em um modelo experimental de desmielinizacao em ratos.

Antioxidant and anti-inflammatory effects of quercetin in functional and morphological alterations in streptozotocin-induced diabetic rats

The aim of this study was to investigate functional and morphological alterations caused by oxidative stress in streptozotocin (STZ)-induced diabetic rats and to evaluate the antioxidant effect of quercetin (QUE) in this disease. One hundred and thirty male Wistar rats, it were randomly distributed in 10 different experimental groups, with ten animals per group: Control Saline (CS), Control Ethanol (CE), Control QUE 5mg/kg (CQ5), Control QUE 25mg/kg (CQ25), Control QUE 50mg/kg (CQ50), Diabetic Saline (DS), Diabetic Ethanol (DE), Diabetic QUE 5mg/kg (DQ5), Diabetic QUE25 mg/kg (DQ25), Diabetic QUE 50mg/kg (DQ50). Therefore, hyperglycemia is directly involved in oxidative stress production, as well as in functional and morphological alterations caused by the excess of free radicals. QUE, specially at the dosage of 50mg/kg, can act as an antioxidant and anti-inflammatory agent, becoming a promising adjuvant in the treatment of diabetes mellitus.

Leishmaniose visceral (Calazar): cinco casos em cães de Santa Maria, Rio Grande do Sul, Brasil

Five canine cases of visceral leishmaniasis were diagnosed. All five dogs presented with icterus, intermitent fever, vomition, anorexia and emaciation. The most prominent gross lesions were hemorrhagic gastroenteritis, interstitial pneumonia and splenomegaly. In tissue sections, free and intracellular forms of Leishmania spp were depicted in macrophages and endothelial cells of all organs scanned. Epidemiological survey to detect either the agent or the sandfly was negative.

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 microL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 +/- 0.77 for oligodendrocytes and 0.67 +/- 0.5 for Schwann cells) compared to non-diabetic rats (3.27 +/- 0.85 and 1.38 +/- 0.81, respectively).

Amniotic Fluid Derived Stem Cells with a Renal Progenitor Phenotype Inhibit Interstitial Fibrosis in Renal Ischemia and Reperfusion Injury in Rats

Objectives Mesenchymal stem cells derived from human amniotic fluid (hAFSCs) are a promising source for cellular therapy, especially for renal disorders, as a subpopulation is derived from the fetal urinary tract. The purpose of this study was to evaluate if hAFSCs with a renal progenitor phenotype demonstrate a nephroprotective effect in acute ischemia reperfusion (I/R) model and prevent late stage fibrosis. Methods A total of 45 male 12-wk-old Wistar rats were divided into three equal groups;: rats subjected to I/R injury and treated with Chang Medium, rats subjected to I/R injury and treated with hAFSCs and sham-operated animals. In the first part of this study, hAFSCs that highly expressed CD24, CD117, SIX2 and PAX2 were isolated and characterized. In the second part, renal I/R injury was induced in male rats and cellular treatment was performed 6 hours later via arterial injection. Functional and histological analyses were performed 24 hours, 48 hours and 2 months after treatment using serum creatinine, urine protein to creatinine ratio, inflammatory and regeneration markers and histomorphometric analysis of the kidney. Statistical analysis was performed by analysis of variance followed by the Tukey’s test for multiple comparisons or by nonparametric Kruskal-Wallis followed by Dunn. Statistical significance level was defined as p <0.05. Results hAFSCs treatment resulted in significantly reduced serum creatinine level at 24 hours, less tubular necrosis, less hyaline cast formation, higher proliferation index, less inflammatory cell infiltration and less myofibroblasts at 48h. The treated group had less fibrosis and proteinuria at 2 months after injury. Conclusion hAFSCs contain a renal progenitor cell subpopulation that has a nephroprotective effect when delivered intra-arterially in rats with renal I/R injury, and reduces interstitial fibrosis on long term follow-up.

Ethidium bromide-induced demyelination of the sciatic nerve of adult Wistar rats

Peripheral nerve ultrastructure was assessed after single or multiple local injections of the intercalating dye ethidium bromide. Thirty-four adult Wistar rats of both sexes were divided into five groups and maintained in a controlled environment with rat chow and water ad libitum throughout the experiment. The experimental animals were injected with 1 microl of 0.1% ethidium bromide in 0.9% saline into the central third of the left sciatic nerve 1 (group 1), 2 (group 2), 4 (group 3), 6 (group 4) or 8 (group 5) times. In groups 2 to 5 the injections were made at 28-day intervals. Control animals received the same amount of 0.9% saline. The animals were killed at different times after injection: group 1 at 7 days (2 rats) and 15 days (2 rats); for groups 2, 3, 4 and 5, all rats were killed 10 days after the last injection and the lesions were investigated by light and transmission electron microscopy. In the acute lesions, intoxicated Schwann cells showed a vacuolated cytoplasm and separation of the sheaths from the axon. Myelin sheaths underwent progressive vesiculation and subsequent segmental demyelination. Myelin debris were withdrawn by macrophages and remyelination by Schwann cells was prominent. With the increase in the number of injections collagen fibers also increased in number and progressively enveloped smaller numbers of remyelinated axons composing new fascicles. Wallerian degeneration of fibers apparently not affected by ethidium bromide was more intense in the nerves from groups 4 and 5. The peripheral nerve repairs itself after demyelinating challenges with a profusion of collagen fibers and new fasciculations. This experimental model is valid to mimic recurrent demyelinating neuropathies.