scholarly journals Acute Toxicity and Cholinesterase Inhibition in Chicks Dosed Orally with Organophosphate Insecticides

2008 ◽  
Vol 59 (3) ◽  
pp. 145-151 ◽  
Author(s):  
Fouad Mohammad ◽  
Yasser Al-Badrany ◽  
Mohammed Al-Jobory

Acute Toxicity and Cholinesterase Inhibition in Chicks Dosed Orally with Organophosphate InsecticidesAcute toxic effects of three commonly used insecticidal preparations of the organophosphates chlorpyrifos, diazinon, and dichlorvos were examined in mixed breed broiler chicks, and cholinesterase activity in plasma and brain were measured. The acute (24 h) oral median lethal doses (LD50) of chlorpyrifos, diazinon, and dichlorvos were 10.79 mg kg-1, 6.32 mg kg-1, and 6.30 mg kg-1, respectively, as determined by the up-and-down method in chicks. Signs of cholinergic toxicosis in the chicks appeared within two hours after dosing, and they included salivation, lacrimation, gasping, frequent defecation, drooping of wings, tremors, convulsions, and recumbency before death. Halving the oral LD50 of chlorpyrifos (5 mg kg-1), diazinon (3 mg kg-1), and dichlorvos (3 mg kg-1) caused immobility and wing drooping, but not the clinical signs of cholinergic toxicity. However, at full LD50 doses of these insecticides, chicks showed clinical signs of cholinergic toxicity similar to those seen in the LD50 experiments. Two out of six chicks died within two hours after treatment with LD50 doses of chlorpyrifos and dichlorvos, whereas LD50 dosing with diazinon caused death in three out of six chicks. Compared to control values, the insecticides reduced plasma and whole brain cholinesterase activities by 29 % to 84 % and 18 % to 77 %, respectively, depending on the dose. The decrease in plasma cholinesterase correlated well (r = 0.82) with that of the brain. These data suggest that organophosphate insecticides administered orally at LD50 doses induce clinical signs of cholinergic poisoning and concurrently reduce brain and plasma cholinesterase activities in chicks.

2011 ◽  
Vol 62 (4) ◽  
pp. 317-323 ◽  
Author(s):  
Muna Al-Zubaidy ◽  
Yaareb Mousa ◽  
Mohammad Hasan ◽  
Fouad Mohammad

Acute Toxicity of Veterinary and Agricultural Formulations of Organophosphates Dichlorvos and Diazinon in ChicksFormulation components of organophosphate insecticidal preparations might affect their toxic action in animals. The objective of this study was to examine and compare the acute toxicity and cholinesterase inhibition in seven to 14-day-old chicks dosed orally with dichlorvos and diazinon in standard veterinary and agricultural formulations. The acute (24 h) oral median lethal doses (LD50) of the formulations were determined using the up-and-down method. Respective LD50 of dichlorvos of the veterinary and agricultural formulations in chicks were 11.1 mg kg-1 and 6.51 mg kg-1 and those of diazinon 6.4 mg kg-1 and 6.7 mg kg-1. Plasma and brain cholinesterase activities were measured by electrometry after in vivo and in vitro exposure to organophosphates. The chicks showed signs of cholinergic toxicosis within one hour of dosing. Dichlorvos (8 mg kg-1) and diazinon (4 mg kg-1) in the veterinary and agricultural formulation significantly reduced both plasma and brain cholinesterase activities in the chicks. The veterinary formulation of dichlorvos reduced plasma ChE by 60 % and agricultural by 40 % and brain ChE by 93 % and 87 %, respectively. In contrast, ChE inhibition by diazinon in the agricultural formulation of diazinon was stronger than by the veterinary formulation; 72 % vs. 64 % in plasma and 97 % vs. 80 % in the brain, respectively. The highest in vitro inhibitions were observed with dichlorvos in the agricultural formulation (50 %) in the brain samples and with diazinon in the agricultural formulation (52 %) in the plasma samples. While they exist, differences between formulations cannot be taken as a rule and further investigations should inventory the toxicity of standard veterinary and agricultural organophosphate formulations in addition to the known data for pure forms.


2014 ◽  
Vol 50 (4) ◽  
pp. 291-295 ◽  
Author(s):  
Taemi Horikawa ◽  
Edward MacKillop ◽  
Anne Bahr

A 13 mo old mixed-breed dog was referred for acute lateralized forebrain signs. MRI of the brain demonstrated abnormalities consistent with severe meningitis and subdural empyema secondary to a retrobulbar abscess. The dog’s clinical signs improved with antibiotic therapy, and repeat imaging showed resolution of subdural fluid accumulation presumed to be empyema with mild residual meningeal enhancement. Subdural empyema is an infrequent cause of encephalopathy in small animals and usually develops through direct extension of a pericranial infection. This report presents a case of presumptive subdural empyema in a dog that was successfully treated without surgical intervention. MRI is the preferred imaging modality for diagnosis of subdural empyema, and the characteristic imaging features are described.


2002 ◽  
Vol 46 (8) ◽  
pp. 2420-2426 ◽  
Author(s):  
Karl V. Clemons ◽  
Raymond A. Sobel ◽  
Paul L. Williams ◽  
Demosthenes Pappagianis ◽  
David A. Stevens

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.


Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 682
Author(s):  
Matthias Christen ◽  
Nils Janzen ◽  
Anne Fraser ◽  
Adrian C. Sewell ◽  
Vidhya Jagannathan ◽  
...  

A 7-month-old, spayed female, domestic longhair cat with L-2-hydroxyglutaric aciduria (L-2-HGA) was investigated. The aim of this study was to investigate the clinical signs, metabolic changes and underlying genetic defect. The owner of the cat reported a 4-month history of multiple paroxysmal seizure-like episodes, characterized by running around the house, often in circles, with abnormal behavior, bumping into obstacles, salivating and often urinating. The episodes were followed by a period of disorientation and inappetence. Neurological examination revealed an absent bilateral menace response. Routine blood work revealed mild microcytic anemia but biochemistry, ammonia, lactate and pre- and post-prandial bile acids were unremarkable. MRI of the brain identified multifocal, bilaterally symmetrical and T2-weighted hyperintensities within the prosencephalon, mesencephalon and metencephalon, primarily affecting the grey matter. Urinary organic acids identified highly increased levels of L-2-hydroxyglutaric acid. The cat was treated with the anticonvulsants levetiracetam and phenobarbitone and has been seizure-free for 16 months. We sequenced the genome of the affected cat and compared the data to 48 control genomes. L2HGDH, coding for L-2-hydroxyglutarate dehydrogenase, was investigated as the top functional candidate gene. This search revealed a single private protein-changing variant in the affected cat. The identified homozygous variant, XM_023255678.1:c.1301A>G, is predicted to result in an amino acid change in the L2HGDH protein, XP_023111446.1:p.His434Arg. The available clinical and biochemical data together with current knowledge about L2HGDH variants and their functional impact in humans and dogs allow us to classify the p.His434Arg variant as a causative variant for the observed neurological signs in this cat.


2016 ◽  
Vol 37 (4) ◽  
pp. 1919
Author(s):  
Átilla Holanda de Albuquerque ◽  
Régis Siqueira de Castro Teixeira ◽  
Débora Nishi Machado ◽  
Elisângela De Souza Lopes ◽  
Ruben Horn Vasconcelos ◽  
...  

Several cases of animal and human salmonellosis caused by the Salmonella serotype Typhimurium have been reported. In animals, subclinical infection favors pathogen dissemination through feces. In this context, the domestic pigeon (Columba livia) with an asymptomatic condition may play an important role in the transmission of salmonellosis, through the elimination of contaminated feces in commercial aviaries or in poultry feed facilities, causing economic losses to the poultry industry and presenting a risk to public health. This study aimed to evaluate the mortality, clinical signs and the presence of Salmonella Typhimurium in the feces and organs of chicks previously inoculated with bacteria isolated from a pigeon. One-day-old chicks were distributed in two experimental groups (G1 and G2) of 32 birds each, and a control group of six birds. Two inocula of 0.4 and 0.7 mL with 105 and 106 colony forming units were used in G1 and G2 birds, respectively. At 1, 4, 7 and 14 days post-inoculation (dpi) fecal samples were pooled from each cage and individual cloacal swabs were collected. At 14 dpi, all chicks were euthanized and samples were collected from the liver, spleen, lung, cecum and intestine for microbiological analysis. Mortality was only observed among G2 birds (6.25%). Most birds presented clinical signs of diarrhea at 4 dpi and no symptom as observed at 14 dpi. The results from cloacal swabs demonstrated bacterial elimination in 68.8% and 53.1% of G2 and G1 birds, respectively at 1 dpi. Additionally, fecal samples had elevated bacterial shedding in all four periods of observation , with a higher excretion at 4 dpi (62.5%) for both groups. Among G2 birds, 74.2% were positive for the pathogen in the intestine; G1 birds presented the lowest rate of lung infection (29%), and both groups had more than 50% positivity for liver and caeca. The results revealed that infected chicks with a Salmonella Typhimurium strains isolated from pigeons may host the pathogen in several organs, and simultaneously present diarrheic disorders with significant levels of bacterial excretion in feces.


1979 ◽  
Vol 51 (5) ◽  
pp. 587-596 ◽  
Author(s):  
Albert N. Martins ◽  
Ralph E. Severance ◽  
James M. Henry ◽  
Thomas F. Doyle

✓ The authors have designed an experiment to detect a hitherto unrecognized interaction between high doses of the glucocorticoid, dexamethasone, and brain irradiation. Eighteen juvenile male rhesus monkeys received 1800 rads to the whole brain in 8.5 minutes. For 1½ days before and 10½ days after the irradiation, nine animals received approximately 2.9 mg/kg/day of dexamethasone intramuscularly in addition to irradiation, while the remaining nine animals served as the control group and received saline. All animals eventually developed a progressive neurological syndrome, and died of delayed radiation necrosis of the brain. The two groups were compared with regard to latency to onset of clinical signs, survival time, and number, distribution, and location of lesions of radionecrosis. Large doses of dexamethasone did not alter the susceptibility of the primate brain to delayed radiation necrosis. Detailed morphological study of the radionecrotic lesions supports the hypothesis that most, if not all, of the lesions develop as the consequence of injury to blood vessels.


1977 ◽  
Vol 56 (1) ◽  
pp. 103-116 ◽  
Author(s):  
M.S. Chi ◽  
C.J. Mirocha ◽  
H.J. Kurtz ◽  
G. Weaver ◽  
F. Bates ◽  
...  

2018 ◽  
Vol 48 (2) ◽  
Author(s):  
Welden Panziera ◽  
Ronaldo Michel Bianchi ◽  
Paula Reis Pereira ◽  
Mariana Martins Flores ◽  
Monique Togni ◽  
...  

ABSTRACT: This report described clinical, epidemiological, and pathological aspects of ischemic myelopathy caused by fibrocartilaginous embolism (FCE) in a 10-year-old, mixed breed gelding. Clinically, the horse presented acute hind limbs paralysis, with a clinical course of approximately 24 hours. At necropsy, no gross lesions were observed. Cross-sections of the spinal cord revealed focally extensive areas of malacia from the T10 to L4 segments. Focally extensive areas of liquefactive necrosis involving the gray matter and adjacent white matter were observed on histologic sections. The lumen of multiple blood vessels in the periphery of the necrotic areas was occluded by fibrocartilaginous emboli that strongly stained with alcian blue. Clinical signs, gross necropsy, and histological findings observed in this case were identical to those described in the literature for ischemic myelopathy caused by FCE in the horse and other species.


2019 ◽  
Vol 47 ◽  
Author(s):  
Viviane Motta dos Santos Moretto ◽  
Luciana Maria Curtio Soares ◽  
Esthefanie Nunes ◽  
Uiara Hanna Araújo Barreto ◽  
Valéria Régia Franco Sousa ◽  
...  

Background: Cerebral cavernous hemangioma is a rare neoplasm of vascular origin in the brain, characterized by abnormally dilated vascular channels surrounded by endothelium without muscle or elastic fibers. Presumptive diagnosis is performed by magnetic resonance or computed tomography (CT) scanning and can be confirmed by histopathology. The prognosis of intracranial cavernous hemangioma is poor, with progression of clinical signs culminating in spontaneous death or euthanasia. The purpose of this paper is to report a case of cerebral cavernous hemangioma in a dog, presenting the clinical findings, tomographic changes, and pathological findings.Case: This case involved a 2-year-old medium sized mixed breed female dog presenting with apathy, hyporexia, ataxia, bradycardia, dyspnea, and seizure episodes for three days. Hemogram and serum biochemistry of renal and hepatic function and urinalysis did not reveal any visible changes. CT scanning was also performed. The scans revealed a hyperdense nodule of 15.9 x 14 mm, with well defined borders, and a hypodense halo without post-contrast enhancement and mass effect in the right parietal lobe was observed in both transverse and coronal sections. Based on the image presented in the CT scans, the nodule was defined as a hemorrhagic brain lesion. The animal died after a seizure. The right telencephalon was subjected to necropsy, which revealed a reddish-black wel-defined nodule 1.7 cm in diameter extending from the height of the piriform lobe to the olfactory trine at the groove level and extending towards the lateral ventricle, with slight compression and deformation of the thalamus but no other macroscopic alterations in the other organs. The histopathology indicated that this nodular area in the encephalus contained moderate, well-delimited but unencapsulated cellularity, composed of large vascular spaces paved with endothelial cells filled with erythrocytes, some containing eosinophilic fibrillar material (fibrin) and others with organized thrombus containing occasional neutrophil aggregates. The endothelial cells had cytoplasm with indistinct borders, elongated nuclei, scanty crust-like chromatin, and cellular pleomorphism ranging from discrete to moderate, without mitotic figures.Discussion: The histological findings characterized the morphological changes in the brain as cavernous hemangioma, and the growth and compression of this neoplasm were considered the cause of the clinical signs of this dog. The main complaint was seizures, although ataxia and lethargy were also noted. These clinical signs are often related to changes in the anterior brain and brainstem. The literature does not list computed tomography as a complementary diagnostic method in cases of cerebral cavernous hemangioma in dogs, but CT scanning was useful in confirming cerebral hemorrhage. The main differential diagnosis for cerebral cavernous hemangioma would be a hamartoma, but what differentiates them histologically is the presence of normal interstices between the blood vessels, since no intervening neural tissue occurs in the case of cerebral hemangioma. Therefore, even in the absence of immunohistochemistry to more confidently confirm a cavernous hemangioma, the clinical signs, CT scans and especially the pathological findings were consistent with a case of cerebral cavernous hemangioma, a benign neoplasm with a poor prognosis due to the severe neurological changes it causes and its difficult treatment.


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