Epizootic Infection by Trypanosoma vivax in Cattle from the State of Minas Gerais, Brazil.

Trypanosomiasis is caused by a pathogenic protozoan of the genus Trypanosoma, being Trypanosoma vivax the most important agent for cattle. The aim of the present study was to demonstrate the expansion of T. vivax infection in different mesoregions of Minas Gerais, Brazil, and describe the clinicopathological findings of trypanosomiasis in cattle. The diagnosis was based on visualization of the parasite in blood smears and DNA detection of T. vivax in the blood of live cows and tissues of necropsied animals by the polymerase chain reaction (PCR). Thirty suspected herds were tested, of which 11 were positive for T. vivax. The most frequent clinical signs were anemia, apathy, drop in milk production, weight loss, reproductive disorders, and nervous signs. Concomitant diseases, such as malignant edema, pneumonia and increased cases of mastitis were associated with T. vivax infection. Three cows were necropsied and the most significant findings were low body condition score, pale mucous and spleen with white pulp hyperplasia. The results demonstrated the expansion of T. vivax infection in Minas Gerais, that PCR-associated blood smears are promising for diagnosis, and that other diseases often occur concomitantly to T. vivax infection in regions with trypanosomiasis in cattle.

Increase in cardiac troponin I in a lamb with tetralogy of fallot.

This study describes a case of tetralogy of Fallot in a lamb showing failure to thrive and signs of respiratory distress. Physical examination, electrocardiography, thoracic radiographies, echocardiography and cardiac troponin I evaluation were performed. The value of cardiac troponin I was compared with the values of 10 healthy lambs of the same age and breed, and the affected animal demonstrated an increase in cardiac troponin I. Due to the poor prognosis, euthanasia was indicated, and necropsy confirmed the diagnosis. This is the first report of an increase in cardiac troponin I in a lamb with tetralogy of Fallot.

Treadmill exercise protects against pentylenetetrazol-induced seizures and oxidative stress after traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of acquired epilepsy, and significant resources are required to develop a better understanding of the pathologic mechanism as targets for potential therapies. Thus, we decided to investigate whether physical exercise after fluid percussion injury (FPI) protects from oxidative and neurochemical alterations as well as from behavioral electroencephalographic (EEG) seizures induced by subeffective convulsive doses of pentylenetetrazol (PTZ; 35 mg/kg). Behavioral and EEG recordings revealed that treadmill physical training increased latency to first clonic and tonic-clonic seizures, attenuated the duration of generalized seizures, and protected against the increase of PTZ-induced Racine scale 5 weeks after neuronal injury. EEG recordings also revealed that physical exercise prevented PTZ-induced amplitude increase in TBI animals. Neurochemical analysis showed that exercise training increased glutathione/oxidized glutathione ratio and glutathione levels per se. Exercise training was also effective against alterations in the redox status, herein characterized by lipid peroxidation (thiobarbituric acid reactive substances), protein carbonyl increase, as well as the inhibition of superoxide dismutase and Na⁺,K⁺-ATPase activities after FPI. On the other hand, histologic analysis with hematoxylin and eosin revealed that FPI induced moderate neuronal damage in cerebral cortex 4 weeks after injury and that physical exercise did not protect against neuronal injury. These data suggest that the ability of physical exercise to reduce FPI-induced seizures is not related to its protection against neuronal damage; however, the effective protection of selected targets, such as Na⁺/K⁺-ATPase elicited by physical exercise, may represent a new line of treatment for post-traumatic seizure susceptibility.

An outbreak of aflatoxin poisoning in dogs associated with aflatoxin B1-contaminated maize products.

An aflatoxicosis outbreak affected 65 dogs from 9 different farms after they were fed diets with cooked corn meal as a common ingredient. Of the dogs, 60 died. Numerous dogs died on additional farms, but those dogs were not included in the study. The farmers acquired the contaminated maize products, in the form of whole corn grain or as corn meal, from the same supplier. The corn product was mixed with meat that was left over from home or commercial rations to form corn polenta, which was fed to the dogs. Necropsy was performed on 3 dogs. Two of the dogs died after a few days of refusing food, showing anorexia, polydipsia, icteric mucous membranes, hematemesis, hematochezia, or melena, and bleeding of the skin, eye, ear, and mouth. The primary necropsy findings included jaundice, hemorrhages in several organs, and yellowish enlarged liver with enhanced lobular pattern. The dog that experienced chronic ascites had a yellowish liver with reduced volume, irregular surface, and increased consistency. The main histological findings included hepatocyte fatty degeneration, biliary duct hyperplasia, cholestasis and, in the chronic case, hepatic fibrosis. High-performance liquid chromatography analysis of the corn meal from 2 affected farms revealed 1,640 ppb and 1,770 ppb of aflatoxin B1, respectively. The current study demonstrates an additional way that dogs can be exposed to, poisoned, and killed by aflatoxin.

Acute and repeated-doses (28 days) toxicity study of Hypericum polyanthemum Klotzsch ex Reichardt (Guttiferare) in mice.

Hypericum polyanthemum, a South Brazilian species showed antidepressant-like and antinociceptive effects in rodents. Since limited information is available on the toxicity and safety profile of the Hypericum genus, we therefore investigated whether H. polyanthemum cyclo-hexane extract (POL) treatment could be associated with toxicity in preclinical setting using mice as an experimental model. These toxicity studies were based on the guidelines of the Organization for Economic Cooperation and Development (OECD-guidelines 423 and 407). Animals received POL single dose (2000 mg/kg, p.o.) or daily for 28-days (90, 450 and 900 mg/kg, p.o.). Acute toxicity study did not detect any clinical signs, changes in behavior or mortality. In repeated dose toxicity study, POL affected the body weight gain and induced biochemical, hematological and liver histological changes at 450 and 900 mg/kg. Mice treated with POL 90 mg/kg did not show any toxicity signs. In conclusion H. polyanthemum can be classified as safe (category 5) according to OECD acute toxicity parameters. However, the alterations observed after repeated treatment with high doses suggest that the liver could be the target organ on potential H. polyanthemum toxicity and point to the need of further toxicity studies.

Síndrome urológica felina: 13 casos / Feline urologic syndrome: 13 cases

Treze casos (8,44 porcento) de síndrome urológica felina foram diagnosticados em 154 necropsias de gatos realizadas de 1991 a 1997. Dados epidemiológicos, sinais clínicos, lesöes de necropsia e achados histopatológicos foram revisados. Sete animais eram machos inteiros e seis eram machos castrados. Obstruçäo uretral, hematúria, disúria e distensäo vesical foram os principais sinais clínicos. Os principais achados de necropsia e histopatológicos foram cistite hemorrágica, pielonefrite, edema perirrenal, hidronefrose, necrose tubular e uretrite.