Spring poisoning hazards

Livestock ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 78-85
Author(s):  
Nicola Bates
Keyword(s):  
Treatment Options ◽  
Clinical Signs ◽  
Rapid Onset ◽  
Food Sources ◽  
Poisonous Plants ◽  
Allium Species ◽  
Cardiac Effects ◽  
Conium Maculatum ◽  
Toxic Plants ◽  
Neurological Effects

Poisoning in the spring may occur in livestock from exposure to glyphosate which is used prior to sowing of plant crops or from ingestion of poisonous plants. Glyphosate is of low toxicity but many products contain a carrier which is irritant to tissues. Plant poisoning may occur because other forage is unavailable and hungry animals will eat unpalatable toxic plants if other food sources are scare. Some plants such as bluebell (Hyacinoides species) and ransom (wild garlic, Allium urinsum) grow in profusion in the spring. Bluebells cause gastrointestinal and cardiac effects and Allium species cause anaemia. Some plants are more toxic in the spring as concentrations of toxic compounds are high compared with other times of the year. This is the case with hemlock (Conium maculatum) and water hemlock (Cicuta virosa). Both these plants cause neurological effects and water hemlock, in particular, causes very rapid onset of clinical signs. Spring flowering plants such as Rhododendron and Pieris species are commonly associated with poisoning, particularly in ruminants. Both these species contain grayanotoxins which cause gastrointestinal and cardiac effects. Access to areas where poisonous plants are known to grow should be restricted and good quality forage provided. Treatment options for management of poisoning in livestock are limited and, in some cases, the only sign of exposure is sudden death.

TOXIC PROPERTIES AND INTAKE SYMPTOMS OF SOME WILD PLANTS IN RELATION TO REPORTED FROM THE FOREST OF NORTH WEST SATPUDA REGION OF MAHARASTRA, INDIA

2017 ◽  
Vol 23 (2) ◽  
Author(s):  
SANJAY A. KHAIRNAR
Keyword(s):  
Secondary Phase ◽  
Wild Plants ◽  
Chemical Components ◽  
World Population ◽  
Poisonous Plants ◽  
North West ◽  
Toxic Plants ◽  
Datura Metel ◽  
Croton Tiglium ◽  
Modern Era

In modern era about 80% of the world population depends on herbal alternative system of medicine. Seventy thousand plants are used in medicine and about 2000 plants are used in Indian Ayurveda. The activities of the curative plants are evaluated by their chemical components. Few of them are important as a medicine but also posses poisonous or toxic properties. The toxicity is produced in them due to the synthesis of toxic chemical compounds may be in primary or secondary phase of their life. Most of the users of such medicinal plants in crude form are tribal and peoples living in the forests and their domestic stock . Most of the time these peoples may not aware about the toxicity of such plants used by them and probably get affected sometimes even leads to death. In the study area during the field survey of poisonous plants, information are gathered from the traditional practicing persons, cow boy and from shepherds. About 20 plant species belonging to 17 families are reported as a medicinal as well as toxic. From the available literature, nature of toxic compound and symptoms of their intake on human being are recorded. In the study area the plants like, Abrus precatorious commonly known as a Gunj or Gunjpala, Jatropha curcas , (Biodiesel plant), Croton tiglium (Jamalgota), Citrullus colocynthis (Kadu Indrawan, Girardinia diversifolia (Agya), Mucuna purriens (Khajkuairi), Euphorbia tirucali (Sher), E. ligularia (Sabarkand), Datura metel ( Kala Dhotara), Datura inoxia (Pandhara Dhotara) and Asparagus racemo-sus (Shatavari) etc . are some of the toxic plants used as a medicine and harmful also.

scholarly journals Chemotherapy induced liver toxicity in children with malignant diseases

2018 ◽  
Vol 91 (1) ◽  
pp. 37-41
Author(s):  
Horváth Adrienne ◽  
Papp Zsuzsanna Erzsébet
Keyword(s):  
Liver Injury ◽  
Maintenance Therapy ◽  
Esophageal Varices ◽  
Liver Toxicity ◽  
Lymphoblastic Leukemia ◽  
Treatment Options ◽  
Clinical Signs ◽  
Treatment Strategies ◽  
Malignant Diseases ◽  
Drug Induced

Abstract A broad spectrum of chemotherapy is being used in the therapy of childhood cancers, which may induce liver injury, impairing quality of life and efficacy of the treatment. History of, especially viral, liver diseases may increase toxicity. The aim of the paper is to assess the incidence, type and grade, predisposing factors and treatment options of drug-induced liver injury in children with malignant diseases under cytostatic therapy at the Hemato-Oncology Department of the Pediatric Clinic 2 from Targu-Mures, over a time period spanning from 2012 to 2017. The results of the study may serve as a foundation for such treatment strategies which would enable optimal outcomes with fewer cases of liver toxicity. During this period, we treated 26 patients with acute lymphoblastic leukemia (ALL), two patients with acute myeloblastic leukemia (AML), one patient with lymphoma and seven with solid tumors. We found liver toxicity in 77% of the patients treated for ALL, mainly during the maintenance therapy (65%) with oral 6-mercaptopurine and methotrexate. The most common clinical signs were anorexia, nausea, vomiting, abdominal pain and faltering weight gain. Cholestasis developed in two patients, while hepatocytolysis was the most common observed event (n = 24). Liver fibrosis, hypersplenism, portal hypertension and esophageal varices were found in two patients. One patient required endoscopic ligation of esophageal varices. Elevation of serum bilirubin appeared in two patients, while hypoproteinemia was observed in nine patients. None of the patients developed acute liver failure. We treated liver toxicity with hydration, alkalinization, i.v. Aspatofort, Aminosteril-N Hepa 8%, oral acetylcysteine, silymarin, ursodeoxycholic acid, Liv-52, Sargenor, and Essentiale forte. We found hepatotoxicity in 77% of the ALL patients undergoing chemotherapy, similar results have been published by other authors. Hepatotoxicity may develop through direct hepatic effects of cytostatics, or a preexisting liver disease impairs the metabolism and excretion of the drug, increasing its toxic effects. In our patients hepatotoxicity can be explained mainly by direct liver-injury, previous infections with hepatotropic viruses, such as cytomegalovirus, were detected only in three patients. Liver injury appeared in 77% of our ALL patients; 65% occurred during maintenance therapy with oral 6-mercaptopurine and methotrexate. Close followup of liver function during chemotherapy is mandatory for optimal results.

Breast and endocrine surgery

2014 ◽  
Author(s):  
Asmaa Al-Alaak
Keyword(s):  
Treatment Options ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Breast Disease ◽  
Endocrine Surgery ◽  
Endocrine Disease ◽  
Surgical Disease ◽  
Clinical Presentations ◽  
Basic Facts ◽  
Clinical Signs And Symptoms

One of the main ‘complaints’ about breast disease is that ‘it is all so similar’ and that there are lots of treatment options which can seem confusing at first. The key to understanding breast disease and preparing for questions about it is to keep the basic facts about breast anatomy and pathology to the forefront, learn to recognize key patterns of clinical signs and symptoms, and then match them to the clinical scenario. The EMQs are particularly useful at practising fitting questions into clinical patterns and rehearsing the patterns. Endocrine disease poses its own challenges. Even for a surgeon it is important to understand and recognize the underlying biochemistry and how this affects the clinical presentations. Endocrine surgical disease is much less about anatomy or surgical procedures themselves as it is about understanding how treatment is matched to the pathophysiology of the conditions.

Metastatic feline mammary cancer: prognostic factors, outcome and comparison of different treatment modalities – a retrospective multicentre study

2020 ◽  
pp. 1098612X2096441
Author(s):  
Gonçalo Petrucci ◽  
Joaquim Henriques ◽  
Hugo Gregório ◽  
Gonçalo Vicente ◽  
Justina Prada ◽  
...  
Keyword(s):  
Metastatic Disease ◽  
Adjuvant Treatment ◽  
Imaging Techniques ◽  
Treatment Options ◽  
Clinical Signs ◽  
Stage Iv ◽  
Metronomic Chemotherapy ◽  
Maximum Tolerated Dose ◽  
Treatment Modalities ◽  
Number Of Patients

Objectives Although feline mammary carcinomas (FMCs) are highly metastatic, the literature and treatment options pertaining to advanced tumours are scarce. This study aimed to investigate the clinical outcome of metastatic FMC with or without adjuvant treatment. Methods The medical records of 73 cats with metastatic FMC (stage 4) were reviewed and included in this study. Metastatic disease was detected by distinct imaging techniques (radiography, ultrasound and CT) and confirmed by cytology and/or histopathology. Cats with adjuvant chemotherapy treatment (n = 34) were divided into three groups: group 1 (n = 9) cats receiving maximum tolerated dose chemotherapy; group 2 (n = 15) cats receiving metronomic chemotherapy; and group 3 (n = 10) cats treated with toceranib phosphate. The study endpoints were time to progression (TTP) and tumour-specific survival (TSS). Treatment-related toxicity was evaluated according to the Veterinary Co-operative Oncology Group’s Common Terminology Criteria for Adverse Events version 1.1 (VCOG-CTCAE). Results Overall mean TTP and TSS were 23 and 44 days, respectively. Cats with clinical signs at the time of diagnosis had a lower TSS (14 days) than asymptomatic cats (120 days; P <0.001). Cats with pleural effusion had a lower TSS (16 days) than cats without ( P <0.001). Median TSS was 58, 75 and 63 in groups 1, 2 and 3, respectively ( P = 0.197). Toxicity was observed in 66.7%, 20% and 30% of cats in groups 1, 2 and 3, respectively. Conclusions and relevance To the best of our knowledge, this study includes the highest number of patients with metastatic FMC assessed. Despite the overall poor prognosis, some cats survived >6 months, indicating that adjuvant treatment may be an option to consider in metastatic disease. More studies are warranted for better understanding and management of stage IV patients.

scholarly journals Plants that cause photosensitivity in ruminants in Brazil

2016 ◽  
Vol 37 (4) ◽  
pp. 2009 ◽  
Author(s):  
Sheila Nogueira Ribeiro Knupp ◽  
Leonardo Sidney Knupp ◽  
Franklin Riet-Correa ◽  
Ricardo Barbosa Lucena
Keyword(s):  
Pyrrolizidine Alkaloids ◽  
Clinical Signs ◽  
Mechanisms Of Action ◽  
Diagnostic Methods ◽  
Future Research ◽  
Steroidal Saponins ◽  
Poisonous Plants ◽  
Toxic Compounds ◽  
Toxic Compound ◽  
Ammi Majus

This study aimed to review the mechanisms of action, clinical signs, pathology, and toxic compounds of plants that cause photosensitivity in ruminants. In addition, we sought to clarify the diagnostic methods and prophylaxis of photosensitivity-induced plants. Photosensitizing plants constitute an important group of poisonous plants in Brazil and there are at least seventeen species distributed in nine genera. Some of these plants have well known toxic compounds; in others, the substance responsible for the disease is unknown. In general, the photosensitivity can be classified as primary or secondary. Among the plants causing primary photosensitivity in Brazil, Ammi majus contains furocoumarins, while the compound in Froelichia humboldtiana remains uncertain. The known toxic compounds causing secondary photosensitivity include pyrrolizidine alkaloids, furans sesquiterpenes, triterpenes, and steroidal saponins. In other plants causing secondary photosensitization, including Stryphnodendron spp. and Enterolobium spp., the toxic compound is still unknown. Future research should be conducted in order to determine the various mechanisms of action of each toxic compound to assist the diagnosis of photosensitivity, to develop less toxic or non-toxic cultivars, or even to find new ways of preventing photosensitization.

scholarly journals Acute Oral Toxicity of Pinnatoxin G in Mice

Toxins ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 87 ◽  
Author(s):  
Silvio Sosa ◽  
Marco Pelin ◽  
Federica Cavion ◽  
Fabienne Hervé ◽  
Philipp Hess ◽  
...  
Keyword(s):  
Acute Toxicity ◽  
Nicotinic Acetylcholine Receptors ◽  
Morphological Changes ◽  
Clinical Signs ◽  
Rapid Onset ◽  
Toxicity Study ◽  
Oral Exposure ◽  
Acute Oral Toxicity ◽  
Oral Toxicity ◽  
Acute Toxicity Study

Pinnatoxin G (PnTx-G) is a marine cyclic imine toxin produced by the dinoflagellate Vulcanodinium rugosum, frequently detected in edible shellfish from Ingril Lagoon (France). As other pinnatoxins, to date, no human poisonings ascribed to consumption of PnTx-G contaminated seafood have been reported, despite its potent antagonism at nicotinic acetylcholine receptors and its high and fast-acting toxicity after intraperitoneal or oral administration in mice. The hazard characterization of PnTx-G by oral exposure is limited to a single acute toxicity study recording lethality and clinical signs in non-fasted mice treated by gavage or through voluntary food ingestion, which showed differences in PnTx-G toxic potency. Thus, an acute toxicity study was carried out using 3 h-fasted CD-1 female mice, administered by gavage with PnTx-G (8–450 µg kg−1). At the dose of 220 µg kg−1 and above, the toxin induced a rapid onset of clinical signs (piloerection, prostration, hypothermia, abdominal breathing, paralysis of the hind limbs, and cyanosis), leading to the death of mice within 30 min. Except for moderate mucosal degeneration in the small intestine recorded at doses of 300 µg kg−1, the toxin did not induce significant morphological changes in the other main organs and tissues, or alterations in blood chemistry parameters. This acute oral toxicity study allowed to calculate an oral LD50 for PnTx-G equal to 208 μg kg−1 (95% confidence limits: 155–281 µg kg−1) and to estimate a provisional NOEL of 120 µg kg−1.

scholarly journals A Rare Case of Hemorrhagic Shock: Morel-Lavallée Lesion

2019 ◽  
Vol 3 (4) ◽  
pp. 417-420 ◽  
Author(s):  
Lieke Claassen ◽  
Myriam Franssen ◽  
Erik Robert de Loos
Keyword(s):  
Treatment Options ◽  
Hypovolemic Shock ◽  
Clinical Signs ◽  
Hemodynamic Instability ◽  
Trauma Patients ◽  
Lumbar Region ◽  
Bilateral Pneumothorax ◽  
Contrast Extravasation ◽  
Multiple Rib Fractures ◽  
Degloving Injury

Hemorrhage is a major cause of death among trauma patients. Controlling the bleeding is essential but can be difficult when the source of bleeding remains unidentified. We present a 67-year-old healthy male with a hypovolemic shock after a suicide attempt by jumping from a height. Apart from a bilateral pneumothorax with multiple rib fractures, a femur fracture and spine fractures, computer tomography (CT) revealed a closed, degloving injury of the back, also known as a Morel-Lavallée lesion. Hemodynamic instability due to hemorrhage caused by a Morel-Lavallée lesion in the lumbar region is very rare and easily overlooked. This case demonstrates the importance of clinical signs of Morel-Lavallée, and illustrates the need for total body CTs to exclude other locations of bleeding and to detect contrast extravasation. This report also discusses the possible treatment options for Morel-Lavallée lesions.

scholarly journals Chronic Subclinical Prion Disease Induced by Low-Dose Inoculum

2002 ◽  
Vol 76 (5) ◽  
pp. 2510-2517 ◽  
Author(s):  
Alana M. Thackray ◽  
Michael A. Klein ◽  
Adriano Aguzzi ◽  
Raymond Bujdoso
Keyword(s):  
Brain Tissue ◽  
Prion Disease ◽  
Low Dose ◽  
Clinical Signs ◽  
Rocky Mountain ◽  
Rapid Onset ◽  
Distinct Pattern ◽  
High Dose ◽  
Terminal Disease ◽  
Subclinical Disease

ABSTRACT We have compared the transmission characteristics of the two mouse-adapted scrapie isolates, ME7 and Rocky Mountain Laboratory (RML), in tga20 mice. These mice express elevated levels of PrP protein compared to wild-type mice and display a relatively short disease incubation period following intracerebral prion inoculation. Terminal prion disease in tga20 mice induced by ME7 or RML was characterized by a distinct pattern of clinical signs and different incubation times. High-dose RML inoculated intracerebrally into tga20 mice induced the most rapid onset of clinical signs, with mice succumbing to terminal disease after only 58 ± 3 days. In contrast, high-dose ME7 gave a mean time to terminal disease of 74 ± 0 days. Histological examination of brain sections from prion-inoculated tga20 mice at terminal disease showed that ME7 gave rise to a more general and extensive pattern of vacuolation than RML. Low-dose inoculum failed to induce terminal disease but did cause preclinical symptoms, including the appearance of reversible clinical signs. Some mice oscillated between showing no clinical signs and early clinical signs for many months but never progressed to terminal disease. Brain tissue from these mice with chronic subclinical prion disease, sacrificed at >200 days postinoculation, contained high levels of infectivity and showed the presence of PrPSc. Parallel analysis of brain tissue from mice with terminal disease showed similar levels of infectivity and detectable PrPSc. These results show that high levels of infectivity and the presence of the abnormal isomer of PrP can be detected in mice with subclinical disease following low-dose prion inoculation.

Hemophagocytic Lymphohistiocytosis: Update of Biology and Treatment Options

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. SCI-9-SCI-9
Author(s):  
Alexandra H. Filipovich
Keyword(s):  
T Cells ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Autosomal Recessive ◽  
Hematopoietic Cell Transplantation ◽  
Conflicts Of Interest ◽  
Treatment Options ◽  
Clinical Signs ◽  
The United States ◽  
Activated T Cells ◽  
High Incidence

Abstract Abstract SCI-9 Hemophagocytic lymphohistiocytosis (HLH) is a group of immunodeficiencies characterized by clinical signs and symptoms of extreme inflammation. HLH is now more widely recognized and no longer viewed as a disorder of young children only, as more adults are being diagnosed and treated. HLH is defined by a unique pattern of clinical findings. In addition to fevers, cytopenias, hepatitis, and splenomegaly, markedly increased levels of inflammatory markers in the blood (ferritin and sCD163 reflecting activation of antigen presenting cells; sIL2Ra and neopterin reflecting activation of T cells) constitute the collection of diagnostic criteria. Activation of inflammatory cells within the central nervous system (CNS) is found in approximately 50 percent of children at diagnosis and requires targeted therapy. In many cases immune defects affecting cytotoxicity of T cells and natural killer cells underlie the susceptibility to HLH. Autosomal recessive disorders include perforin deficiency (the major cytotoxin of the immune system), or defects in proteins involved in degranulation and exocytosis of perforin and granzyme B (MUNC 13–4, MUNC18-2, STX11, Rab27a). The latter proteins are involved in degranulation generally within the hematopoietic system, thus impacting the function of neutrophils and platelets as well. A rare defect of granulogenesis, Chediak Higashi syndrome, is also associated with a high incidence of HLH. Two forms of X-linked lymphoproliferative syndrome (XLP1 – SAP deficiency, and XLP2 – XIAP deficiency), as well as the rare autosomal recessive disorder ITK (IL-2 inducible T cell kinase) deficiency, are characterized by a high incidence of Epstein-Barr virus-driven HLH and lymphoproliferation. A common pathogenic mechanism underlying these consequences has not yet been elucidated. Effective initial treatment for HLH consists of cytotoxic and anti-inflammatory agents. The most widely used over the past 20 years has been a combination of CNS-penetrating steroid (Decadron) and etoposide. Another approach has been to use anti-thymocyte globulin (ATG) as induction therapy. Both treatments have resulted in approximately 60 percent responses during the first month of therapy. Supportive care with broad-spectrum antimicrobials is a critical adjunct. More recently, a new induction protocol—hybrid immunotherapy for HLH, combining the features of early ATG followed by etoposide, with steroids—has been opened in the United States (http://clinicaltrials.gov/ct2/show/NCT01104025) and Europe. However, HLH persists or reactivates in nearly half of patients as immune suppression is reduced. While a common approach to reactivation is to reintensify previous therapy, no clear guidelines have been developed for this complication. The use of Campath, a humanized monoclonal anti-CD52 antibody, as salvage therapy prior to hematopoietic cell transplantation (HCT) is being tested, as both activated T cells and activated monocyte/macrophages (histiocytes) are targeted through CD52. Historically, the three-year survival after HCT in patients treated with HLH-94 was 60 percent. More recently, use of Campath-based reduced intensity conditioning protocols have led to improved results after HCT. Campath has the advantage of reducing graft-versus-host disease if properly timed prior to HCT. In a recent contemporaneous series of HCT from unrelated adult donors, three-year posttransplant survival improved from 43 percent to 92 percent with no early transplant-related mortality. Disclosures: No relevant conflicts of interest to declare.

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