scholarly journals Hepatic Encephalopathy Secondary to Chronic Liver Lesions Caused by Crotalaria incana in a Bovine

2019 ◽  
Vol 47 ◽  
Author(s):  
Paula Veloso Leal ◽  
Gleice Kelli Avardes De Melo ◽  
Arnildo Pott ◽  
Tessie Beck Martins ◽  
Dale Gardner ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Clinical Signs ◽  
Chronic Liver ◽  
Human Beings ◽  
Alzheimer Type ◽  
Mato Grosso ◽  
Voucher Specimen ◽  
Toxic Principle ◽  
The Brain

Background: Crotalaria spp. Poisoning induces liver or pulmonary disease. C. mucronata, C. juncea, C. spectabilis, and C. retusa are the Crotalaria spp. inducing spontaneous intoxication in livestock in Brazil. C. mucronata and C. juncea are associated with interstitial pneumonia, while C. retusa and C. specatabilis induce hepatotoxicosis. The toxic principle in Crotalaria spp. are dehydropyrrolizidine alkaloids and their N-oxides. C. incana poisoning to livestock is rarely documented. This paper reports the clinical signs and pathological findings of a case of Crotalaria incana poisoning in a steer. The chemical finding of a potential toxic dehydropyrrolizidine alkaloid in the plant is documented for the first time.Case: The affected bovine was part of a herd of 80 two-year-old steers that were transferred from Property 1 to Property 2, 30 days prior to the event. In the pasture of Property I - where the steers were held for 6 months - there was a heavy infestation by a Crotalaria species with signs of being consumed by the steers. The plant was identified as Crotalaria incana at the Botanical Laboratory of the Federal University of Mato Grosso do Sul and a voucher specimen was filed there under the register GCMS 51169. Two days after entering Property 2 one of the steers became depressed, staggering, and in poor body condition. With time, the steer became oblivious to the environment and died 20 days after the onset of the clinical signs. Significant necropsy findings were limited to the liver which was markedly enlarged and with rounded edges. The hepatic cut surface was mottled with dark red and extensive orange areas of discoloration. The gallbladder was distended and the bile was inspissated. Microscopically, in the liver, there was fibrosis, bile duct hyperplasia and hepatocellular megalocytosis. The Glisson’s capsule was markedly thickened by fibrosis. In the brain, there was vacuolation of myelin sheaths (status spongiosus), moderate gliosis, and rare Alzheimer type 2 astrocytes.Discussion: The diagnosis of intoxication by C. incana was based on clinical signs and pathological changes and the evidence of the plant being consumed. The high infestation of C. incana in the pasture, the high proportion of dead matter and the low concentration of viable pasture favored the ingestion of C. incana. Spongy degeneration, a typical lesion of hepatic encephalopathy, was observed in the several areas of the brain. Cirrhosis of the liver as seen in the case of this report, results in elevated ammonia levels in the blood - and eventually in the brain – and ammonia toxicity causes hepatic encephalopathy. Morphological changes in hepatic encephalopathy in the central nervous system of human beings and horses centers on astrocytes which undergo Alzheimer type 2 change developing an enlarged, pale nuclei with a rim of chromatin and prominent nucleoli. Astrocytes pairs and triplets are seen, and, in severe cases, astrocytic nuclei may become lobulated and contain glycogen. Chemical analysis of C. incana was accomplished by acid-base extraction with zincreduction of N-oxides and quantitation by spectrometry. Quantitative analysis was achieved by liquid chromatography-mass spectrometry. To confirm the identity of the alkaloid in the sample of C. incana the isolated alkaloid was compared to a standard sample of usaramine previously isolated, and its identity verified by magnetic resonance spectroscopy analysis. The 1,2-dehydropyrrolizidine alkaloid usaramine, as well as its  N-oxide, were identified as the major alkaloids in in C. incana. The concentration found in the seed was consistent with that previously reported. This is a new finding on the toxic principle of C. incana. Keywords: cattle diseases, poisonous plants, pathology, hepatotoxicity, Crotalaria incana, chronic liver failure.

scholarly journals Presence of amastigotes in the central nervous system of hamsters infected with Leishmania sp.

2011 ◽  
Vol 20 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Elisangela de Oliveira ◽  
Elisa Teruya Oshiro ◽  
Rebeca Vieira Pinto ◽  
Bruna Corrêa de Castro ◽  
Karla Borges Daniel ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Clinical Signs ◽  
Direct Examination ◽  
Mato Grosso ◽  
The Central Nervous System ◽  
Animal House ◽  
Immunohistochemical Studies ◽  
Negative Controls ◽  
The Brain

Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.

scholarly journals Impaired brain glymphatic flow in a rodent model of chronic liver disease and minimal hepatic encephalopathy

2017 ◽  
Author(s):  
Anna Hadjihambi ◽  
Ian F. Harrison ◽  
Natalia Arias ◽  
Rocío Gallego-Durán ◽  
Patrick S. Hosford ◽  
...  
Keyword(s):  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Minimal Hepatic Encephalopathy ◽  
Brain Regions ◽  
Chronic Liver ◽  
Waste Products ◽  
Cognitive Behavioural ◽  
Contrast Enhanced ◽  
The Brain

AbstractNeuronal function is exquisitely sensitive to alterations in extracellular environment. In patients with hepatic encephalopathy (HE), accumulation of metabolic waste products and noxious substances in the interstitial fluid of the brain may contribute to neuronal dysfunction and cognitive impairment. In a rat model of chronic liver disease, we used an emerging dynamic contrast-enhanced MRI technique to assess the efficacy of the glymphatic system, which facilitates clearance of solutes from the brain. We identified discrete brain regions (olfactory bulb, prefrontal cortex and hippocampus) of altered glymphatic flow, which aligned with cognitive/behavioural deficits. Although the underlying pathophysiological mechanisms remain unclear, this study provides the first experimental evidence of impaired glymphatic clearance in HE.

scholarly journals Association of Type 2 Diabetes and Hepatic Encephalopathy in Chronic Liver Disease Patients

Cureus ◽  
2021 ◽  
Author(s):  
Mohsin A Usmani ◽  
Attiya S Rahman ◽  
Qaiser Jamal ◽  
Muhammad Siddiqui
Keyword(s):  
Type 2 Diabetes ◽  
Liver Disease ◽  
Hepatic Encephalopathy ◽  
Chronic Liver Disease ◽  
Chronic Liver

scholarly journals Hepatic encephalopathy in adult dog secondary to cirrhosis due to congenital biliary agenesis: a case report

2021 ◽  
Vol 15 (2) ◽  
pp. 96-101
Author(s):  
Fernanda Bueno Oliveira ◽  
Thanielle Novaes Fontes ◽  
Marilaine Carlos Sousa ◽  
Ana Caroline da Silva Néto Souza ◽  
Tiago da Cunha Peixoto ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Neurological Disorders ◽  
Incidental Finding ◽  
Clinical Signs ◽  
Aromatic Amino Acids ◽  
Short Chain Fatty Acids ◽  
Pathological Findings ◽  
Chronic Liver Failure ◽  
Gallbladder Agenesis ◽  
The Brain

Gallbladder agenesis is a congenital malformation that is considered extremely rare in dogs. The disease can course asymptomatically or with clinical signs, usually non-specific and including vomiting, anorexia, diarrhea, ascites, and lethargy. The objective of this report was to describe the clinical and anatomopathological aspects of a dog with hepatic encephalopathy secondary to gallbladder agenesis. This condition can be diagnosed during surgery or imaging examinations; however, it is often an incidental finding. In the biochemical examinations, a decrease in alanine aminotransferase and an increase in alkaline phosphatase and hypoalbuminemia were observed. During the necropsy, hepatomegaly was observed with absence of the gallbladder, congestion, cerebral edema, lipiduria, and pulmonary edema. Microscopically, there was intense fibrosis and inflammation in the liver due to chronic cholangiohepatitis (cirrhosis of the liver). The consequence of this lesion secondary to gallbladder agenesis was hepatic encephalopathy. Chronic liver failure exposes the cerebral cortex to toxins that are not metabolized by the liver, such as ammonia, mercaptans, short-chain fatty acids, scatols, indols, and aromatic amino acids. These toxins cause reversible damage to the brain, which results in neurological disorders. In this report, the dog had no clinical neurological signs, and the diagnosis of this condition was observed histologically. Dogs with gallbladder agenesis usually have clinical and pathological findings of hepatobiliary lesions such as cholestasis, cholangiohepatitis, and, in severe cases, hepatic encephalopathy, which are necessary to differentiate from other diseases that affect the hepatobiliary system, such as cholelithiasis, neoplasms, and chronic hepatitis.

scholarly journals Bacopa monnieriExtract (CDRI-08) Modulates the NMDA Receptor Subunits and nNOS-Apoptosis Axis in Cerebellum of Hepatic Encephalopathy Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Papia Mondal ◽  
Surendra Kumar Trigun
Keyword(s):  
Nitric Oxide ◽  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Apoptosis Pathway ◽  
Nitric Oxide Level ◽  
Nmdar Activation ◽  
Oxide Synthase ◽  
The Brain

Hepatic encephalopathy (HE), characterized by impaired cerebellar functions during chronic liver failure (CLF), involves N-methyl-D-aspartate receptor (NMDAR) overactivation in the brain cells.Bacopa monnieri(BM) extract is a known neuroprotectant. The present paper evaluates whether BM extract is able to modulate the two NMDAR subunits (NR2A and NR2B) and its downstream mediators in cerebellum of rats with chronic liver failure (CLF), induced by administration of 50 mg/kg bw thioacetamide (TAA) i.p. for 14 days, and in the TAA group rats orally treated with 200 mg/kg bw BM extract from days 8 to 14. NR2A is known to impart neuroprotection and that of NR2B induces neuronal death during NMDAR activation. Neuronal nitric oxide synthase- (nNOS-) apoptosis pathway is known to mediate NMDAR led excitotoxicity. The level of NR2A was found to be significantly reduced with a concomitant increase of NR2B in cerebellum of the CLF rats. This was consistent with significantly enhanced nNOS expression, nitric oxide level, and reduced Bcl2/Bax ratio. Moreover, treatment with BM extract reversed the NR2A/NR2B ratio and also normalized the levels of nNOS-apoptotic factors in cerebellum of those rats. The findings suggest modulation of NR2A and NR2B expression by BM extract to prevent neurochemical alterations associated with HE.

scholarly journals Reactivation of latent bovine herpesvirus type 5 in cattle with polioencephalomalacia induced by ammonium sulphate

2007 ◽  
Vol 27 (10) ◽  
pp. 435-441 ◽  
Author(s):  
Nadia David ◽  
Sílvia O. Hübner ◽  
Franklin Riet-Correa ◽  
Danisa Halfen ◽  
Ricardo A. Lemos
Keyword(s):  
Ammonium Sulphate ◽  
Clinical Signs ◽  
Uninfected Control ◽  
Mato Grosso ◽  
Herpesvirus Type ◽  
Nasal Swabs ◽  
The Central Nervous System ◽  
The Brain ◽  
Bovine Herpesvirus Type 5 ◽  
Mato Grosso Do Sul

In the state Mato Grosso do Sul, Brazil, outbreaks of meningoencephalitis by BoHV-5 and polioencephalomalacia (PEM) display similar epidemiological features, suggesting that meningoencephalitis may be associated with reactivation of a latent BoHV-5 infection, during the development of PEM. To test this hypothesis, four 7-8 months old steers negative for BoHV-5 antibodies were inoculated intranasally with BoHV-5 and received amprolium from day 35 to day 105 after inoculation. Because PEM was not produced during this period, ammonium sulphate was given from day 114 to day 180 after inoculation. Two uninfected control steers received amprolium and ammonium sulphate for the same periods. All inoculated cattle developed antibodies against BoHV-5 after inoculation and the virus was isolated from nasal swabs, indicating that they were infected. Two inoculated steers had clinical signs of PEM after 118 and 146 days after virus inoculation. One was euthanized after a clinical manifestation period of seven days and had severe lesions of PEM and meningoencephalitis. BoHV-5 was isolated from the central nervous system of this animal. The other animal recovered but continued to manifest chronic signs of PEM and was euthanatized. On histological examination, the cerebral cortex, caudate nucleus and thalamus had multifocal areas of malacia and mild meningoencephalitis of the cortex. BoHV-5 was not isolated from the brain. One uninfected control steer had signs of neurological disease on day 158 and had lesions of PEM without meningoencephalitis at necropsy. The simultaneous production of PEM and diffuse meningoencephalitis, with isolation of BoHV-5, in one steer treated with ammonium sulphate, 118 days after BoHV-5 inoculation, suggests that latent BoHV-5 was reactivated in this animal submitted to experimental induction of PEM.

MRI findings in two West Highland White Terrier dogs with hepatic encephalopathy secondary to portosystemic shunt

2019 ◽  
Vol 7 (3) ◽  
pp. e000814 ◽  
Author(s):  
Ricardo Fernandes ◽  
Colin Driver ◽  
J H Rose ◽  
Clare Rusbridge
Keyword(s):  
Hepatic Encephalopathy ◽  
Vascular System ◽  
Clinical Signs ◽  
Systemic Circulation ◽  
Brain Parenchyma ◽  
Portosystemic Shunt ◽  
Medial Longitudinal Fasciculus ◽  
Mri Findings ◽  
Weighted Sequences ◽  
The Brain

A portosystemic shunt is an abnormal communication between the portal vascular system and the systemic circulation. A significant number of clinical signs associated with portosystemic shunting result from hepatic encephalopathy (HE); a syndrome encompassing neurological signs such as including changes in behaviour, ataxia, unresponsiveness, pacing, circling, blindness, seizures, coma and death. We present two West Highland White Terrier dogs diagnosed with HE based on clinical signs, bile acid stimulation test and imaging of the abnormal vessel communicating the portal and the systemic circulation. Magnetic resonance sequences of the brain revealed a poorly marginated and diffuse, bilateral and symmetric hyperintense lesions on T2-weighted, fluid attenuation inversion recovery and diffusion-weighted sequences relative to the brain parenchyma including the medial longitudinal fasciculus and reticular formation in the brainstem. No abnormalities were detected on T1-weighted sequences.

TEORI KECERDASAN, PENDIDIKAN ANAK, DAN KOMUNIKASI DALAM KELUARGA

1970 ◽  
Vol 6 (1) ◽  
Author(s):  
Muskinul Fuad
Keyword(s):  
Multiple Intelligences ◽  
Educational Activity ◽  
Howard Gardner ◽  
Human Beings ◽  
Brain Functions ◽  
Starting Point ◽  
The Family ◽  
Education Today ◽  
The Brain ◽  
Spatial Logics

The education system in Indonesia emphasize on academic intelligence, whichincludes only two or three aspects, more than on the other aspects of intelligence. For thatreason, many children who are not good at academic intelligence, but have good potentials inother aspects of intelligence, do not develop optimally. They are often considered and labeledas "stupid children" by the existing system. This phenomenon is on the contrary to the theoryof multiple intelligences proposed by Howard Gardner, who argues that intelligence is theability to solve various problems in life and produce products or services that are useful invarious aspects of life.Human intelligence is a combination of various general and specific abilities. Thistheory is different from the concept of IQ (intelligence quotient) that involves only languageskills, mathematical, and spatial logics. According to Gardner, there are nine aspects ofintelligence and its potential indicators to be developed by each child born without a braindefect. What Gardner suggested can be considered as a starting point to a perspective thatevery child has a unique individual intelligence. Parents have to treat and educate theirchildren proportionally and equitably. This treatment will lead to a pattern of education that isfriendly to the brain and to the plurality of children’s potential.More than the above points, the notion that multiple intelligences do not just comefrom the brain needs to be followed. Humans actually have different immaterial (spiritual)aspects that do not refer to brain functions. The belief in spiritual aspects and its potentialsmeans that human beings have various capacities and they differ from physical capacities.This is what needs to be addressed from the perspective of education today. The philosophyand perspective on education of the educators, education stakeholders, and especially parents,are the first major issue to be addressed. With this step, every educational activity andcommunication within the family is expected to develop every aspect of children'sintelligence, especially the spiritual intelligence.

scholarly journals Efficacy of Intravenous Liposomal Amphotericin B (AmBisome) against Coccidioidal Meningitis in Rabbits

2002 ◽  
Vol 46 (8) ◽  
pp. 2420-2426 ◽  
Author(s):  
Karl V. Clemons ◽  
Raymond A. Sobel ◽  
Paul L. Williams ◽  
Demosthenes Pappagianis ◽  
David A. Stevens
Keyword(s):  
Spinal Cord ◽  
Amphotericin B ◽  
Liposomal Amphotericin ◽  
White Blood Cells ◽  
Clinical Signs ◽  
Liposomal Amphotericin B ◽  
Coccidioides Immitis ◽  
Lower Protein ◽  
Motor Abnormalities ◽  
The Brain

ABSTRACT The efficacy of intravenously administered liposomal amphotericin B (AmBisome [AmBi]) for the treatment of experimental coccidioidal meningitis was compared with those of oral fluconazole (FLC) and intravenously administered conventional amphotericin B (AMB). Male New Zealand White rabbits were infected by intracisternal inoculation of arthroconidia of Coccidioides immitis. Starting 5 days postinfection, animals received one of the following: 5% dextrose water diluent; AMB given at 1 mg/kg of body weight; AmBi given at 7.5, 15, or 22.5 mg/kg intravenously three times per week for 3 weeks; or oral FLC given at 80 mg/kg for 19 days. One week after the cessation of therapy, all survivors were euthanatized, the numbers of CFU remaining in the spinal cord and brain were determined, and histological analyses were performed. All AmBi-, FLC-, or AMB-treated animals survived and had prolonged lengths of survival compared with those for the controls (P < 0.0001). Treated groups had significantly lower numbers of white blood cells and significantly lower protein concentrations in the cerebrospinal fluid compared with those for the controls (P < 0.01 to 0.0005) and had fewer clinical signs of infection (e.g., weight loss, elevated temperature, and neurological abnormalities including motor abnormalities). The mean histological scores for AmBi-treated rabbits were lower than those for FLC-treated and control rabbits (P < 0.016 and 0.0005, respectively); the scores for AMB-treated animals were lower than those for the controls (P < 0.0005) but were similar to those for FLC-treated rabbits. All regimens reduced the numbers of CFU in the brain and spinal cord compared with those for the controls (P ≤0.0005). AmBi-treated animals had 3- to 11-fold lower numbers of CFU than FLC-treated rabbits and 6- to 35-fold lower numbers of CFU than AmB-treated rabbits. Three of eight animals given 15 mg of AmBi per kg had no detectable infection in either tissue, whereas other doses of AmBi or FLC cleared either the brain or the spinal cord of infection in fewer rabbits. In addition, clearance of the infection from both tissues was achieved in none of the rabbits, and neither tissue was cleared of infection in AMB-treated animals. Overall, these data indicate that intravenously administered AmBi is superior to oral FLC or intravenous AMB and that FLC is better than AMB against experimental coccidioidal meningitis. These data indicate that AmBi may offer an improvement in the treatment of coccidioidal meningitis. Additional studies are warranted.

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