A Case Report of Successful Treatment of Minoxidil Toxicosis Using Hemodialysis in a Cat.

A 5-year-old castrated male American Shorthair cat presented with lethargy and anorexia after accidentally knocking over a bottle of topical minoxidil and spilling it onto its body. Physical examination revealed rapid shallow breathing, pale mucous membranes, hypothermia, tachycardia, and hypotension. Thoracic radiography revealed mild pulmonary infiltration and pleural effusion. Despite conservative treatment, including oxygen therapy, and intravenous fluid, furosemide, and dopamine administration, the patient showed no improvement. After two sessions of intermittent hemodialysis, the cat's respiratory pattern and overall condition gradually improved; normal body temperature and blood pressure were achieved. The cat recovered fully and was discharged on the 11th day of hospitalization. This is the first report on the use of hemodialysis in the treatment of a cat with minoxidil toxicosis.

An in vitro evaluation of intravenous lipid emulsion on three common canine toxicants.

Objective: To determine whether intravenous lipid emulsion (ILE) therapy significantly reduces the concentration of baclofen, ibuprofen, and/or bromethalin in canine whole blood over time. Animals: Seven 500 mL bags of canine DEA 1.1 negative blood were divided into aliquots of 125 mL and randomly assigned to one of three treatment groups (baclofen, ibuprofen, bromethalin) or four control groups (a positive control for each treatment group and a negative control group). Procedures: Injectable ibuprofen (200 mg/kg), baclofen (8 mg/kg), or bromethalin (3 mg/kg) was apportioned into 125 mL aliquots of canine whole blood and incubated for 30 min at 38.5°C. ILE (12.4 mL, Intralipid® ) was added to each sample and the solution vortexed [215 rpm for 15 min at 37°C (98.6°F)]. Samples were obtained at designated time points (0, 15, 30, 60, 180, 360 min), centrifuged, and separated into serum and RBC fractions. Serum samples were ultracentrifuged (22,000 g for 10 min at 37°C) to separate lipid rich and poor fractions. Samples were stored at -80°C prior to analysis. Results: A significant decrease in total drug concentration was established for bromethalin and its metabolite desmethylbromethalin compared to positive controls. ILE significantly reduced desmethylbromethalin at the 30-and 360-min time points. The remainder of the desmethylbromethalin time points did not reach significance. Bromethalin concentration was significantly reduced at all time points compared to positive controls. Neither baclofen nor ibuprofen had significant changes in concentration. Conclusion: ILE therapy was effective at reducing the total drug concentration of bromethalin and its metabolite desmethylbromethalin supporting the lipid sink theory. As a single compartment in vitro study, this study does not evaluate other proposed mechanisms of action of ILE therapy. ILE therapy may have other means of significantly decreasing lipophilic drug concentration in cases of toxicosis.

"Flux in the Belly:" A History of Infantile Gastroenteritis.

BACKGROUND: Although a major cause of infant mortality for centuries, little research was done on the causes of infants' diarrhea. Artificial feeding, teething, and summer heat were believed to cause the severe disease that spared breastfed infants. SUMMARY: Since antiquity, infants' digestive disorders were termed dyspepsia, flux of the belly, diarrhea, gastroenteritis, watery gripes, the runs, dysentery, or cholera, without definitions. Alois Bednar discerned 3 grades (dyspepsia, diarrhea, and cholera) of the same disease. Infants' neurologic symptoms were interpreted as alimentary toxicosis. Chronic diarrhea caused emaciation and dehydration. In 1950, Laurence Finberg found diarrhea with hypernatremia causing cerebral damage. Seasonal influence was known since Hippocrates. Baudelocque recommended obtaining infant milk fresh from the cow because it decomposes in the summer heat. In the cities, summer diarrhea caused a third of total infant mortality. Physicians debated whether heat acted directly on the infant or spoiled the food. The discovery of microorganisms in the 1860s revolutionized medical understanding. However, influential researchers such as Adalbert Czerny classified nutritional disturbances by assumed pathogenesis ("ex alimentation, ex infection, ex constitution"), but denied the possibility of bacterial infection via milk. Heating baby food, practiced for centuries, was introduced in Denmark, Sweden, and France, whereas in Britain and Germany, professional and public debate on pasteurization persisted. KEY MESSAGES: It took half a century to implement effective hygienic measures once the bacterial origin became known. Foodborne infection was rejected, and the prejudice that raw milk possesses essential "living" properties, adopted by influential scientists, contributed to delaying pasteurization.

Exploring the impacts of fescue toxicosis on the pulmonary arterial pressure of angus cows.

Vasoconstriction of peripheral blood vessels is one of the hallmark symptoms of fescue toxicosis in cattle. Thus, it was hypothesized that exposure to ergot alkaloids would increase the pulmonary arterial pressure (PAP). The objectives of this study were to examine the relationship between PAP and different physiological parameters of cows grazing either endophyte-infected (EI) or novel-endophyte (EN) fescue, then evaluate changes in PAP and other physiological measurements in cows exposed to EI pastures and deemed as susceptible or tolerant based on animal performance. Pregnant Angus cows at 2 different locations grazed either EI or EN fescue pastures for 14 consecutive weeks starting in early April of 2022. Forage measurements were collected to assess ergot alkaloid exposure throughout the study. In addition to measuring PAP, weekly measurements and blood samples were collected to evaluate physiological responses to ergot alkaloid consumption. The Fescue Toxicosis Selection Method (FTSM) was used for a post hoc analysis to identify cattle as either tolerant (EI-TOL) or susceptible (EI-SUS) when challenged with ergot alkaloid exposure. Data were analyzed using a MIXED procedure of SAS with repeated measures. Cows grazing on EN pastures had greater mean PAP values than EI cows, (P < 0.01), whereas a location effect was identified when comparing both EI-TOL and EI-SUS groups (P < 0.01). Cows exposed to EN pastures had greater average daily gain (ADG) (P = 0.04) and progesterone (P4) concentrations (P < 0.01), and lower hair shedding scores (HSS; P < 0.01) than EI cows. The EI-TOL cows tended to have greater final body weight, ADG and had lower HSS (P < 0.01) than EI-SUS cows. While cattle consuming EI tall fescue exhibited classical physiological changes, the decrease in PAP of cattle consuming EI fescue was unexpected and contradicted the initial hypothesis. Furthermore, the FTSM provides a means to identify animals with superior performance in spite of the chronic exposure to ergot alkaloids. Continued investigations examining the interaction between ergot alkaloid exposure and cardiovascular parameters will lead to a fuller understanding of the disease and are pivotal for developing innovative strategies that enhance best management practices to help guarantee the sustainability of the U.S. beef industry.

Since ergot alkaloids were identified as the causative agent of fescue toxicosis in cattle that grazed on endophyte-infected tall fescue pastures, multiple studies have been designed to understand the disease and develop strategies to minimize its negative effects on cattle performance. One of the major consequences of this disease is vasoconstriction, which alters the normal functioning of the cardiovascular system. Therefore, the objective of this study was to examine the relationship between pulmonary arterial pressure (PAP) and different physiological parameters of cows exposed to ergot alkaloids. The evaluation of the interaction between PAP and fescue toxicosis is innovative to beef cattle research in the United States. The results obtained in this study provide a new perspective to analyze the impact of ergot alkaloids on the cardiopulmonary system of cattle and demonstrates that this multifaceted disease demands a multifaceted research approach.

Transferring knowledge across aquatic species via clustering techniques to unravel patterns of pesticide toxicity.

In silico modelling takes the advantage of accelerating ecotoxicological assessments on hazardous chemicals without conducting risky in vivo experiments under ethic regulation. To date, the prevailing strategy of one model for one species cannot be well generalized to multi-species modelling. In this work, we propose a new strategy of one model for multiple species to facilitate knowledge transfer across aquatic species. The available lethal concentration values of 4952 pesticides on 651 fish species are aggregated into one toxicity response matrix, purely through which we attempt to unravel fish toxicosis-phylogenesis relationships and pesticide toxicity-structure relationships via clustering techniques including non-negative matrix factorization (NMF) and hierarchical clustering. The clustering results suggest that (1) close NMF weights indicate close species-toxicosis and pesticide-toxicity profiles; (2) and that species toxicosis patterns are related with species phylogenetic relationships; (3) and that close pesticide-toxicity profiles indicate similar atom-pair structural fingerprints. These environmental, chemical and biological insights can be used as expert knowledge for environmentalists to manually gain knowledge about untested species/pesticides from tested species/pesticides, and meanwhile provide support for us to build in silico models from species phylogenetic and pesticide structural points of view. Besides unravelling the mechanisms behind toxicity response, we also adopt stratified cross validation and external test to validate the reliability of using NMF to predict missing toxicity values. Independent test on external data shows that NMF achieves 0.8404-0.9397 R2 on four fish species. In the context of toxicity prediction, non-negative matrix factorization can be viewed as a model based on quantitative activity-activity relationships (QAAR), and provides an alternative approach of inferring toxicity values on untested species from tested species.

Impact of endophyte-infected tall fescue seed consumption on endocrine changes associated with intake regulation and post-absorptive metabolism in growing steers.

Fescue toxicosis is a syndrome occurring from the consumption of endophyte-infected tall fescue and results in substantial economic losses to the beef industry primarily from reduced growth accompanied by decreased dry matter intake (DMI); however, the associations characterizing this reduction in DMI have yet to be elucidated. The objective of this experiment was to identify endocrine changes associated with intake regulation post-consumption of endophyte-infected tall fescue seed (E+). Twelve Holstein steers were stratified by body weight and assigned to 1 of 3 treatments (n=4): 0 ppm ergovaline (ERV), 1.8 ppm ERV, or 2.7 ppm ERV. Treatments were achieved by combining differing proportions of ground E+ and non-endophyte-infected tall fescue seed. Steers were adapted to their diets for 7 d followed by a 7 d DMI collection period. Within treatment, steers were assigned to a sampling day (d 16 or d 17). Blood samples were collected every 20 min for 8 h, beginning 1 h before feeding. Intake data was analyzed using the MIXED procedure of SAS 9.4 (SAS Inst. Inc., Cary, NC) with treatment, day, and the interaction as fixed effects. Hormone and metabolite data were analyzed with the fixed effect of treatment, time, and the interaction including time as a repeated measure and orthogonal contrasts. Dry matter intake was linearly decreased with increasing ERV in the diet (P < 0.001). Insulin and leptin concentrations exhibited a quadratic effect (P = 0.018 and P = 0.005) with insulin concentrations highest for the 2.7 ppm treatment and leptin concentrations highest for the 1.8 ppm treatment. No differences were detected for active ghrelin or ß-hydroxybuytrate concentrations among treatment groups. Further, steers consuming both the 1.8 and 2.7 ppm ERV treatments had lower prolactin concentrations compared to the 0 ppm treatment (quadratic, P= 0.019). Glucose concentrations had a tendency for a linear increase as ERV concentrations increased (P = 0.091). A treatment × time interaction (P = 0.002) was noted in NEFA concentrations, with the 1.8 ppm ERV treatment showing increased pre-feeding concentrations, and the 2.7 ppm ERV treatment exhibiting elevated NEFA concentrations as time post-feeding progressed. The results suggest that E+ consumption reduces intake likely through alterations in intake-related hormones and post-absorptive metabolism and contributes to our current understanding of E+ effects on intake reduction while providing avenues for future research.

Suppression of inositol pyrophosphate toxicosis and hyper-repression of the fission yeast PHO regulon by loss-of-function mutations in chromatin remodelers Snf22 and Sol1.

Inositol pyrophosphates are signaling molecules that regulate cellular phosphate homeostasis in eukaryal taxa. In fission yeast, where the phosphate regulon (comprising phosphate acquisition genes pho1, pho84, and tgp1) is repressed under phosphate-replete conditions by lncRNA-mediated transcriptional interference, mutations of inositol pyrophosphatases that increase IP8 levels derepress the PHO regulon by eliciting precocious termination of lncRNA transcription. Asp1 pyrophosphatase mutations resulting in too much IP8 are cytotoxic in YES medium owing to overexpression of glycerophosphodiester transporter Tgp1. IP8 toxicosis is ameliorated by mutations in cleavage/polyadenylation and termination factors, perturbations of the Pol2 CTD code, and mutations in SPX domain proteins that act as inositol pyrophosphate sensors. Here, we show that IP8 toxicity is alleviated by deletion of snf22+, the gene encoding the ATPase subunit of the SWI/SNF chromatin remodeling complex, by an ATPase-inactivating snf22-(D996A-E997A) allele, and by deletion of the gene encoding SWI/SNF subunit Sol1. Deletion of snf22+ hyper-repressed pho1 expression in phosphate-replete cells; suppressed the pho1 derepression elicited by mutations in Pol2 CTD, termination factor Seb1, Asp1 pyrophosphatase, and 14-3-3 protein Rad24 (that favor precocious prt lncRNA termination); and delayed pho1 induction during phosphate starvation. RNA analysis and lack of mutational synergies suggest that Snf22 is not impacting 3'-processing/termination. Using reporter assays, we find that Snf22 is important for the activity of the tgp1 and pho1 promoters, but not for the promoters that drive the synthesis of the PHO-repressive lncRNAs. Transcription profiling of snf22∆ and snf22-(D996A-E997A) cells identified an additional set of 66 protein-coding genes that were downregulated in both mutants.IMPORTANCERepression of the fission yeast PHO genes tgp1, pho1, and pho84 by lncRNA-mediated interference is sensitive to inositol pyrophosphate dynamics. Cytotoxic asp1-STF alleles derepress the PHO genes via the action of IP8 as an agonist of precocious lncRNA 3'-processing/termination. IP8 toxicosis is alleviated by mutations of the Pol2 CTD and the 3'-processing/termination machinery that dampen the impact of toxic IP8 levels on termination. In this study, a forward genetic screen revealed that IP8 toxicity is suppressed by mutations of the Snf22 and Sol1 subunits of the SWI/SNF chromatin remodeling complex. Genetic and biochemical evidence indicates that the SWI/SNF is not affecting 3'-processing/termination or lncRNA promoter activity. Rather, SWI/SNF is critical for firing the PHO mRNA promoters. Our results implicate the ATP-dependent nucleosome remodeling activity of SWI/SNF as necessary to ensure full access of PHO-activating transcription factor Pho7 to its binding sites in the PHO mRNA promoters.

Identification of Candidate Protein Biomarkers Associated with Domoic Acid Toxicosis in Cerebrospinal Fluid of California Sea Lions (Zalophus californianus).

Since 1998, California sea lion (Zalophus californianus) stranding events associated with domoic acid toxicosis (DAT) have consistently increased. Outside of direct measurement of domoic acid in bodily fluids at the time of stranding, there are no practical nonlethal clinical tests for the diagnosis of DAT that can be utilized in a rehabilitation facility. Proteomics analysis was conducted to discover candidate protein markers of DAT using cerebrospinal fluid from stranded California sea lions with acute DAT (n = 8), chronic DAT (n = 19), or without DAT (n = 13). A total of 2005 protein families were identified experiment-wide. A total of 83 proteins were significantly different in abundance across the three groups (adj. p < 0.05). MDH1, PLD3, ADAM22, YWHAG, VGF, and CLSTN1 could discriminate California sea lions with or without DAT (AuROC > 0.75). IGKV2D-28, PTRPF, KNG1, F2, and SNCB were able to discriminate acute DAT from chronic DAT (AuROC > 0.75). Proteins involved in alpha synuclein deposition were over-represented as classifiers of DAT, and many of these proteins have been implicated in a variety of neurodegenerative diseases. These proteins should be considered potential markers for DAT in California sea lions and should be prioritized for future validation studies as biomarkers.

A Novel TSHR Gene Mutation in a Family with Non-autoimmune Hyperthyroidism.

Background: Familial non-autoimmune hyperthyroidism is a rare disorder characterized by the absence of thyroid autoimmunity, particularly TSH receptor antibody [TRAb]. Objective: The aim of this study was to describe a novel TSHR mutation identified in a family of two siblings and their father. Methods: Two siblings presented for endocrine assessment at ages 7 and 14 years with mild T3 toxicosis, and the father presented at 30 years of age with non-autoimmune thyrotoxicosis. Both siblings were treated with oral antithyroid therapy to achieve reasonable symptom control and thyroid function normalization. The father was treated with oral antithyroid therapy, radioactive iodine, thyroidectomy, and thyroid replacement therapy. Peripheral blood DNA was extracted from both affected siblings and father. Mutation analysis of TSHR was carried out by PCR and Sanger sequencing of both strands of the extracted DNA. Results: Both siblings and their father were heterozygous for the missense TSHR variant c.1855G>C, p.[Asp619His], in exon 10. Conclusions: This novel TSHR variant is associated with T3 toxicosis during childhood. Therefore, early identification and treatment may improve patient outcomes.

The effects of CDP-choline treatment in Amanita phalloides mushroom toxicosis.

Amanita phalloides poisoning is known to be the most fatal case among mushroom poisoning cases. Its main mechanism of toxicity is that it leads to cell death by the irreversible binding of its toxins to the DNA-dependent RNA polymerase II enzyme. This study was planned to analyze the effects of the CDP-choline molecule on Amanita phalloides mushroom poisoning cases. The extract of the Amanita phalloides mushroom was taken and intraperitoneally administered to male Wistar Albino rats at a dose of 0.3 g/kg. In the experiment phase, the rats were divided into three groups of CDP-choline treatment according to the doses of 100 mg/kg, 250 mg/kg, and 500 mg/kg, and one control group was administered a 1 ml/kg dose of 0.9% isotonic NaCl solution. The treatments were then administered intraperitoneally at the 2nd hour, and at the 6th hour, the rats were sacrificed. The degree of damage in the liver and kidney tissues of the rats was evaluated histopathologically. It was concluded that CDP-choline reduced or prevented the damage that occurred in the liver significantly and dose-dependently in the toxicosis picture caused by Amanita phalloides, and it showed a tendency to lower or prevent the damage in the kidney, albeit not significantly.

Toxigenic Endophyte-Infected Tall Fescue and Ergot Alkaloids.

"Fescue toxicosis" and reproductive ergotism present identical toxidromes in late-gestational mares and, likely, other equids. Both toxic syndromes are caused by ergopeptine alkaloids (EPAs) of fungal origin, and they are collectively referred to as equine ergopeptine alkaloid toxicosis (EEPAT). EPAs are produced by either a toxigenic endophyte (Epichloë coenophiala) in tall fescue and/or a nonendophytic fungus (Claviceps purpurea), infecting small grains and grasses. EEPAT can cause hypoprolactinemia-induced agalactia/dysgalactia, prolonged gestation, dystocia, and other reproductive abnormalities in mares, as well as failure of passive transfer in their frequently dysmature/overmature/postmature foals. Prevention relies on eliminating exposures and/or reversing hypoprolactinemia.

Copper-associated chronic hepatitis in Cavalier King Charles spaniels.

BACKGROUND: Copper-associated chronic hepatitis (CuCH) is poorly characterised in Cavalier King Charles spaniels (CKCS). METHODS: Hepatic copper accumulation was qualitatively and quantitatively assessed, and blood samples were used for genetic testing to screen for known CuCH-associated genetic variants. RESULTS: The study included 13 CKCS with CuCH and eight unaffected controls. Increased transaminase activities, elevated biliary enzyme concentrations and portal hypertension were documented in 100%, 73% and 38% of dogs with CuCH, respectively. Five dogs had three or more abnormalities in measures of liver function. All 11 dogs with CuCh that underwent genetic testing were homozygous negative for the COMMD1 deletion and ATP7A variant but homozygous positive (n = 7) or heterozygous (n = 4) for the ATP7B variant. Liver histology often demonstrated marked architectural distortion by severe, bridging fibrosis and regenerative nodules with lymphoplasmacytic inflammation. Centrilobular copper accumulation characterised early cases with minimal fibrosis. When fibrosis was significant, copper was often differentially concentrated within regenerative nodules. Chelation therapy resolved laboratory derangements and portal hypertension in five of seven dogs. Of the 7 non-surviving dogs with CuCH, 6 had not received chelation therapy. LIMITATIONS: Limitations include a small cohort size and the lack of pedigree analyses to corroborate heritability. CONCLUSIONS: CuCH should be considered in CKCS with suspected liver disease. Long-term prognosis seems favourable in dogs receiving chelation therapy, notwithstanding the presence of previously reported negative prognostic markers.

An experimental study of consecutive administration of ropinirole and apomorphine for emesis induction in dogs.

OBJECTIVE: To study the safety and effectiveness of consecutively administered ropinirole and apomorphine (both dopamine 2-like receptor agonists) for emesis induction in dogs. DESIGN: Prospective, crossover study design. SETTING: Institutional animal research facility. ANIMALS: Six healthy male purpose-bred Beagle dogs. INTERVENTIONS: Each dog received 4 treatments: (1) apomorphine infusion (21 µg/kg) over 30 minutes + ropinirole eye drops (3.75 mg/m2 ); (2) ropinirole infusion (108 µg/m2 ) over 30 minutes + apomorphine SC (100 µg/kg); (3) apomorphine SC (100 µg/kg) + ropinirole eye drops (7.5 mg/m2 ) after 30 minutes; and (4) ropinirole eye drops (7.5 mg/m2 ) + apomorphine SC (100 µg/kg) after 30 minutes. Infusions were administered via a catheter instrumented in the cephalic vein. Eye drops and SC injections were administered as described in the product inserts. Blood samples were taken for ropinirole and apomorphine concentration analysis before dosing and periodically following administrations. The washout period between the treatments was 5-7 days. MEASUREMENTS AND MAIN RESULTS: Number of vomits and clinical signs were recorded. Alertness and heart rate were monitored in conjunction with blood sampling. The average number of vomits varied between 4.3 and 8.8 (range 1-16) following treatments. Signs of nausea, vomiting, and lethargy were seen in all individuals without significant differences between treatments. Moderate to marked, transient increase in heart rates was detected in all treatments. Infrequent noted side effects included ocular hyperemia, blepharospasms, and muscle tremors. Prior treatment with apomorphine significantly decreased the absorption of ropinirole eye drops. CONCLUSIONS: The safety and efficacy profiles of this experimental study support that ropinirole and apomorphine could be administered consecutively in cases where the treatment using 1 substance has resulted in an incomplete evacuation of the stomach contents, and the attending veterinarian considers the use of a different agent to have benefits that outweigh the risks.

Diagnostic Pathology of Equine Toxicoses.

This article is intended to highlight toxicosis-associated pathology in horses that might be observed by a clinician in the living animal and at gross necropsy. When the clinician is aware of these pathologic changes (particularly when coupled with a suggestive environmental or herd history), then collaboration with a diagnostic laboratory can begin to help identify specific toxicants. Proper sampling and communication with the diagnostic laboratory will vastly improve the likelihood of a specific diagnosis; postmortem sampling and specimen submission are reviewed in the last section of this article.

Ruminal ergovaline and volatile fatty acid dynamics: Association with poor performance and a key growth regulator in steers grazing toxic tall fescue.

Fescue toxicosis (FT) is produced by an ergot alkaloid (i.e., ergovaline [EV])-producing fungus residing in toxic fescue plants. Associations between EV, decreased weight gain and ruminal volatile fatty acids are unclear. Feces, rumen fluid, and blood were collected from 12 steers that grazed non-toxic (NT) or toxic (E +) fescue for 28 days. The E + group exhibited decreased propionate (P), increased acetate (A), and increased ruminal A:P ratio, with similar trends in feces. Plasma GASP-1 (G-Protein-Coupled-Receptor-Associated-Sorting-Protein), a myostatin inhibitor, decreased (day 14) only in E + steers. Ergovaline was present only in E + ruminal fluid and peaked on day 14. The lower ruminal propionate and higher A:P ratio might contribute to FT while reduced GASP-1 might be a new mechanism linked to E + -related weight gain reduction. Day 14 ergovaline zenith likely reflects ruminal adaptations favoring EV breakdown and its presence only in rumen points to local, rather than systemic effects.

The symptomatology and diagnosis of domoic acid toxicosis in stranded California sea lions (Zalophus californianus): a review and evaluation of 20 years of cases to guide prognosis.

Introduction: Domoic acid (DA) is a glutaminergic excitatory neurotoxin that causes the morbidity and mortality of California sea lions (Zalophus californianus; CSL) and other marine mammals due to a suite of effects mostly on the nervous and cardiac systems. Between 1998 and 2019, 11,737 live-stranded CSL were admitted to The Marine Mammal Center (TMMC; Sausalito, CA, USA), over 2,000 of which were intoxicated by DA. A plethora of clinical research has been performed over the past 20 years to characterize the range of toxic effects of DA exposure on CSLs, generating the largest dataset on the effects of natural exposure to this toxin in wildlife. Materials and methods: In this study, we review published methods for diagnosing DA intoxication, clinical presentation, and treatment of DA-intoxicated CSL and present a practical, reproducible scoring system called the neuroscore (NS) to help assess whether a DA-affected CSL is fit for release to the wild following rehabilitation. Logistic regression models were used to assess the relationships between outcome (released vs. euthanized or died) and multiple variables to predict the outcome for a subset of 92 stranded CSLs. Results: The largest proportion of DA-intoxicated CSLs was adult females (58.6%). The proportions of acute and chronic cases were 63.5 and 36.5% respectively, with 44% of affected CSL released and 56% either dying naturally or euthanized. The average time in rehabilitation was 15.9 days (range 0-169) for all outcomes. The best-performing model (85% accuracy; area under the curve = 0.90) assessing the relationship between outcome and predictor variables consisted of four variables: final NS, change in NS over time, whether the animal began eating in rehabilitation, and the state of nutrition on admission. Discussion: Our results provide longitudinal information on the symptomatology of CSL intoxicated by domoic acid and suggest that a behavioral scoring system is a useful tool to assess the fitness for the release of DA-intoxicated CSL.

Trace Mineral Nutrition in Confinement Dairy Cattle.

Veterinarians are often called upon to diagnose health-related issues on the farm that may be related to trace mineral deficiencies or toxicities. Trace mineral feeding rates are often not available due to the proprietary nature of the trace mineral premixes provided by nutritional consultants. The veterinarian needs to be aware of the common clinical signs of trace mineral deficiencies and toxicities, interactions between trace minerals that may result in deficiencies, clinical samples that are necessary for the proper diagnosis, and the recommended normal ranges of each trace mineral depending on the age of the animal.

Clinical Outcomes of the Deleterious Effects of Aluminum on Neuro-Cognition, Inflammation, and Health: A Review.

Introduction: In the scenario of metal toxicity, aluminum (Al) stands out as a ubiquitous type of metal that can be combined with other elements and form different compounds. Al is widely used daily as an adjuvant in vaccines, antacids, food additives (as components of AI-containing food additives), skin care products, cosmetics, and kitchenware, and can be an element or contaminant present in our daily life. Objective: To present a review of the main deleterious effects of Al on human health. Methods: The search was carried out from September 2022 to February 2023 in the Scopus, PubMed, Science Direct, Scielo, and Google Scholar databases, using scientific articles from 2012 to 2023. The quality of the studies was based on the GRADE instrument, and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusions: A total of 115 files were search returned. Further, 95 articles were evaluated, and 44 were included in this review. Based on the results, measuring Al's relevance to health is essential in medicine. Several studies have demonstrated clinical outcomes and metabolic alterations with Al exposure. The tolerable weekly intake established by the European Food Safety Authority (EFSA) of 1 mg Al/kg body weight can be achieved through dietary exposure alone. Proven neurotoxicity in humans is the critical adverse effect of Al. A carcinogenic effect of Al has not been proven so far. Preventive medicine advocates that exposure to Al should be kept as low as possible. Chelating agents, such as calcium disodium ethylene diamine tetraacetic acid and deferoxamine, are options for acute poisoning, and monomethysilanetriol supplementation may be a long-term strategy with chelation potential. Further studies are needed to assess the impacts of Al on human health.

Phenibut toxicosis in a dog.

OBJECTIVE: To describe the successful treatment of severe neurological and cardiovascular abnormalities in a dog following ingestion of the neuropsychotropic drug, phenibut. CASE SUMMARY: A 2-year-old neutered male Weimaraner was found unresponsive and laterally recumbent in his urine after ingesting approximately 1600 mg/kg of phenibut. On presentation to an emergency clinic, the dog was neurologically inappropriate, tachycardic, hypertensive, and exhibiting a profoundly decreased respiratory rate. Because of progressive clinical signs, electrolyte abnormalities, increased hepatic enzyme activity and bilirubin concentrations, and the development of pigmenturia, referral to specialist care was sought. On presentation, the dog was intermittently somnolent and then maniacal. Sinus tachycardia persisted, and hyperthermia was documented. Hospitalization for supportive care was undertaken, and the dog was administered IV fluids, flumazenil, antiepileptics, and IV lipid emulsion therapy. The dog developed hypoglycemia and treated with dextrose supplementation. Progressive increases in liver enzyme activities as well as pronounced increase in creatine kinase activity, consistent with rhabdomyolysis, were noted. Over the course of 48 hours, the hypoglycemia resolved, and clinical signs significantly improved. Ultimately, the dog was discharged with improved clinical signs, with the owner reporting that 1 week after discharge, a full recovery had been made, and no residual clinical signs persisted. NEW INFORMATION PROVIDED: To the authors' knowledge, there are no previous reports of phenibut intoxication in small animals. The growing availability and use of this drug by people in the past several years highlight the need for a greater understanding of its effects in companion animals.

Common Toxicosis.

Veterinarians are often called upon to diagnose health-related issues on the farm that may be related to trace mineral deficiencies or toxicities. Trace mineral feeding rates are often not available due to the proprietary nature of the trace mineral premixes provided by nutritional consultants. The veterinarian needs to be aware of the common clinical signs of trace mineral deficiencies and toxicities, interactions between trace minerals that may result in deficiencies, clinical samples that are necessary for the proper diagnosis, and the recommended normal ranges of each trace mineral depending on the age of the animal.