scholarly journals LABORATORY EXAMINATION IN NERVE AGENT INTOXICATION

2013 ◽  
Vol 56 (3) ◽  
pp. 89-96 ◽  
Author(s):  
Jiří Bajgar

Diagnosis of nerve agent intoxication is based on anamnestic data, clinical signs and laboratory examination. For acute poisoning, cholinesterase activity in the blood (erythrocyte AChE, plasma/serum BuChE) is sensitive, simple and most frequent laboratory examination performed in biochemical laboratories. Specialized examinations to precise treatment (reactivation test) or to make retrospective diagnosis (fluoride induced reactivation etc.) can be conducted. Other sophisticated methods are available, too.

Author(s):  
Irena Bradinova ◽  
Silvia Andonova ◽  
Alexey Savov

AbstractPontocerebellar hypoplasia type 1B is a severe autosomal recessive neurologic disorder characterized by a combination of cerebellar and spinal motor neuron degeneration beginning at birth. Pontocerebellar hypoplasia type 1B is caused by mutations in EXOSC3 gene. High prevalence of the p.Gly31Ala mutation was found recently, especially in the Roma ethnic minority. We present a young Bulgarian Roma family with two deceased newborn children manifesting severe neuromuscular disorder including severe muscle weakness, respiratory distress, and multiple joint contractures. Based on the clinical signs and family's population characteristics, DNA testing for the previously described EXOSC3 in Bulgarian Roma mutation c.92G > C; p.Gly31Ala was performed on blood samples of both parents and they were found to be heterozygous carriers. This finding indirectly confirmed the diagnosis of pontocerebellar hypoplasia type B in the deceased offspring. Knowledge of population-specific molecular bases of genetic conditions was the key to final diagnosis in the presented family. Designing of population-based clinical-genetic panels may be a powerful diagnostic tool for patients with such origin. Preconception carrier screening in high-risk population groups is a feasible option to discuss.


2021 ◽  
Vol 19 ◽  
pp. 107-113
Author(s):  
P. A. Onyeyili ◽  
F. A. Ameh ◽  
B. S. Paul

Toxicity studies of 0,0-diethyl-0-(2- isoprophyl-6-methyl-4-pyrimidinyl) phosphorothioate (DiazinonR) was carried out in the Balami breed of sheep. The agent was administered orally daily for one week at the rate of 20, 25 and 30mg/kg body weight to groups of sheep. The 30mg/kg dose produced transient clinical signs in the sheep. Diazinon inhibited plasma and red blood cell cholinesterase activity. The intensity of the inhibition was more with 30mg/kg dose and occurred as from day 3 and lasted till the end of the investigation 7 days post treatment. Leucocytosis was also observed with the 30mg/kg dose. There was no observable effect of the chemical on the RBC, Hb, and PCV values in sheep at the dosages used.


2012 ◽  
Vol 60 (4) ◽  
pp. 521-527 ◽  
Author(s):  
Yakup Yildirim ◽  
Seval Bilge Dağalp ◽  
Volkan Yilmaz ◽  
Ali Faraji Majarashin

In this study, the physical examination of 22 cattle revealed clinical signs of malignant catarrhal fever (MCF). Peripheral blood leukocyte (PBL) samples of the 22 cattle, and nasal (n = 7) and conjunctival (n = 9) swab samples from 16 sheep from two different farms, were taken for laboratory examination. The clinical diagnosis of MCF in cows was confirmed by the detection of ovine herpesvirus type 2 (OvHV-2) DNA by polymerase chain reaction (PCR). OvHV-2 DNA was detected by nested-PCR in PBL of one cow with clinical signs and nasal (1/7)-conjunctival(1/9) swab samples of two sheep housed in the same barn. According to the sequence analysis, three slightly divergent viruses were detected. The results indicate the need for additional research in different regions of Turkey to gain a better understanding of the incidence of MCF and its implications for the livestock industry.


2016 ◽  
Vol 52 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Christiane Weingart ◽  
Achim D. Gruber ◽  
Mathias Brunnberg ◽  
Barbara Kohn

A 12 yr old female neutered Carthusian crossbreed cat was presented due to progressive neurological signs. Clinical signs included dehydration, stupor, and anisocoria. Laboratory examination revealed severe hypernatremia, azotemia, hyperglobulinemia, and an erythrocytosis. Clinical signs and hypernatremia suggested an intracranial process. Imaging studies revealed a loss of structure in the cerebrum, hypothalamus, and pituitary gland. Due to a poor prognosis, the cat was euthanatized. Histopathological examination revealed a subacute granulomatous and necrotizing panencephalitis with Toxoplasma-typical protozoa. The Toxoplasma-induced dysfunction of the hypothalamus and pituitary gland led to diabetes insipidus, which was, in combination with insufficient water intake, the most likely cause for the hypernatremia.


2010 ◽  
Vol 50 (3) ◽  
pp. 159-160 ◽  
Author(s):  
D R Mahadeshwara Prasad ◽  
Hareesh S Gouda ◽  
Vinay R Hallikeri

Biochemical markers are one of the mainstays in the diagnosis of ill health. Plasma cholinesterase is one such marker of the ill health caused by acute organophosphorus pesticide poisoning. Organophosphorus pesticides are powerful inhibitors of plasma cholinesterase; consequently, the reduced level of this biochemical marker has been used in the diagnosis of cases of acute poisoning. But how dependable is this biochemical marker in the diagnosis of suspected organophosphorus pesticide poisoning without adequate clinical signs and symptoms? In the case reported here, the low level of plasma cholinesterase which was suspected to be due to organophosphorus poisoning was found to be caused by pulmonary Koch's and hepatitis B with associated malnutrition.


2015 ◽  
Vol 58 (4) ◽  
pp. 128-130
Author(s):  
Jiří Bajgar ◽  
Jiří Cabal ◽  
Jiří Kassa ◽  
Michal Pavlík

Background: The method of continual determination of the rat blood cholinesterase activity was developed to study the changes of the blood cholinesterases following different intervetions. Aims: The aim of this study is registration of cholinesterase activity in the rat blood and its changes to demonstrate detoxification capacity of rats to inactivate sarin or VX in vivo. Methods: The groups of female rats were premedicated (ketamine and xylazine) and cannulated to a. femoralis. Continual blood sampling (0.02 ml/min) and monitoring of the circulating blood cholinesterase activity were performed. Normal activity was monitored 1–2 min and then the nerve agent was administered i.m. (2× LD50). Using different time intervals of the leg compression and relaxation following the agent injection, cholinesterase activity was monitored and according to the inhibition obtained, detoxification capacity was assessed. Results: Administration of sarin to the leg, then 1 and 5 min compression and 20 min later relaxation showed that further inhibition in the blood was not observed. On the other hand, VX was able to inhibit blood cholinesterases after this intervention. Conclusions: The results demonstrated that sarin can be naturally detoxified on the contrary to VX. Described method can be used as model for other studies dealing with changes of cholinesterases in the blood following different factors.


2021 ◽  
Vol 51 (10) ◽  
Author(s):  
Igor Ribeiro dos Santos ◽  
Luan Cleber Henker ◽  
Tainah Pereira Dal Pont ◽  
Welden Panziera ◽  
Saulo Petinatti Pavarini ◽  
...  

ABSTRACT: Forty 1-2-y-old water buffaloes were simultaneously treated with trichlorfon and chlorpyrifos products in the recommended dose for cattle. After a week, 19 animals started presenting clinical signs characterized by apathy, diarrhea, aggressiveness, dehydration, and motor incoordination, followed by flaccid paralysis and permanent lateral recumbency. All affected buffaloes died after a clinical course of 1-4 days. Reduction of serum cholinesterase activity in three cases was indicative of significant exposure to organophosphorus compounds (OPs). Pathological examination of three buffaloes revealed no gross and histological lesions. By thin layer chromatography, chlorpyrifos residues and trace of trichlorfon residues were detected in fresh tissue samples. The epidemiological, clinical, pathological, and toxicological findings were highly compatible with OPs-induced delayed neurotoxicity, a neurological manifestation rarely described in domestic animals.


2019 ◽  
Vol 70 (1) ◽  
pp. 1443
Author(s):  
V. TSIOURIS ◽  
A. STARRAS ◽  
I. GEORGOPOULOU ◽  
A. ANGELOU ◽  
E. PAPADOPOULOS

A dead pigeon (Columba livia) was submitted to the Unit of Avian Medicine, Clinic of Farm Animals, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, Greece. It derived from a pigeon flock consisted of approximately 100 racing birds of various ages between 4 months to 5 years old. The flock was kept on a terrace indoors in 4 cages of 3 m2 each. Near this flock, there were also two other pigeon flocks in a distance of 20 and 30 meters, respectively. The pigeons’ health problem had been present in this flock for approximately 3 years before this delivery. Lack of appetite, poor growth of young birds, weakness, depression, vomiting, diarrhea and emaciation were the most important clinical signs of the pigeons in the flock. During necropsy, discoloration and atrophy of liver, spleen and kidneys, edema of gizzard, necrosis in the koilin layer of the gizzard and under this, presence of small parasites, dilatation in the anterior small intestine (duodenum, jejunum) and finally hemorrhagic content in the second half of the small intestine and the rectum were observed. According to the findings of the postmortem and laboratory examination, amidostomosis was determined to be the cause of the pigeon’s death. Although pigeon infection by Amidostomum spp. is reported around the world, so far, amidostomosis has not been reported in pigeons in Greece. Pigeon owners should take all the appropriate treating and managing measures to control the spread of this parasite and its consequences on their flocks.


2021 ◽  
Vol 7 (3) ◽  
pp. 93-100
Author(s):  
Ekaterina S. Karpushkina ◽  
Olga A. Zhdanova ◽  
Galina A. Batishcheva ◽  
Yulia A. Petukhova

Introduction: Acute poisoning by nasal decongestants is an important issue in pediatrics due to physiological and anatomical characteristics of the child’s body and pharmacokinetics of drugs in early childhood. Epidemiology: The number of poisonings by this group of drugs ranged from 4% to 39% during the period from 2000 to 2018. All the studies reported that the most severe degree of intoxication was observed in children aged 1–3 years. Mechanism of action of nasal decongestants: The peculiarity of selective alpha2-adrenergic agonists is that when taken orally, misused or overdosed, they lose their selectivity for the target receptor. As a result, the drug causes acute poisoning and most often this effect occurs in children and adolescents. Clinical features and diagnostic criteria: Clinical signs of acute poisoning can appear both as a result of an overdose of the nasal decongestants and due to a therapeutic use of the drug according to the instruction. The symptoms are manifested by hypothermia, skin pallor, bradycardia, arterial hypotension, profuse sweating, and acrocyanosis. Imidazoline receptors and new opportunities: It is assumed that toxic effect of topical decongestants occurs not only by activation of alpha2-adrenergic receptors, but also through their influence on the selective imidazoline receptors. Based on the structure of these drugs, it is assumed that imidazoline receptors are the primary binding site for these drugs. Conclusion: Understanding the described mechanisms of alpha2-adrenergic agonist action and peculiarities of the child’s symptoms in acute poisoning is necessary for the timely diagnosis and selection of the correct treatment strategy.


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