This retrospective, observational study describes the clinical findings, case management trends, and outcomes of 83 dogs and nine cats exposed to eastern coral snakes in a university teaching hospital setting. The medical records of dogs and cats that received antivenom following coral snake exposure were reviewed. Data collected included signalment, time to antivenom administration, physical and laboratory characteristics at presentation, clinical course during hospitalization, length of hospitalization, and survival to discharge. The mean time from presentation to coral snake antivenom administration was 2.26 ± 1.46 h. Excluding cases where the owner declined in-hospital care, the mean hospitalization time for dogs and cats was 50.8 h and 34 h, respectively. The mean number of antivenom vials was 1.29 (1-4). Gastrointestinal signs (vomiting and ptyalism) occurred in 42.2% (35/83) of dogs and 33.3% (3/9) of cats. Peripheral neurologic system deficits (ataxia, paresis to plegia, absent reflexes, and hypoventilation) were noted in 19.6% (18/92) of dogs and cats. Hemolysis was also common in 37.9% (25/66) of dogs but was not observed in cats. Mechanical ventilation (MV) was indicated in 12% (10/83) of dogs but no cats. Acute kidney injury (AKI), while rare, was a common cause of euthanasia at 20% (2/5) and was the most common complication during MV at 44.4% (4/9). Pigmenturia/hemolysis occurred in 88.9% (8/9) of MV cases and in all cases with AKI. Despite delays in antivenom administration by several hours, dogs and cats with coral snake exposure have low mortality rates (6% of dogs (5/83) and 0% of cats). Gastrointestinal signs were common but were not predictive of progression to neurological signs. Thus, differentiating between coral snake exposure and envenomation before the onset of neurological signs remains challenging.

Domoic acid (DA) is a naturally occurring marine neurotoxin produced by Pseudo-nitzschia diatoms. Adult California sea lions (Zalophus californianus) can experience multiple post-exposure syndromes, including acute toxicosis and chronic epilepsy. Additionally, a delayed-onset epileptic syndrome is proposed for California sea lions (CSL) exposed in utero. This brief report explores a case of a CSL developing adult-onset epilepsy with progressive hippocampal neuropathology. Initial brain magnetic resonance imaging (MRI) and hippocampal volumetric analyses relative to brain size were normal. Approximately 7 years later, MRI studies to evaluate a newly developed epileptic syndrome demonstrated unilateral hippocampal atrophy. While other causes of unilateral hippocampal atrophy cannot be completely excluded, this case may represent in vivo evidence of adult-onset epileptiform DA toxicosis in a CSL. By estimating in utero DA exposure time period, and extrapolating from studies conducted on laboratory species, this case provides circumstantial evidence for a neurodevelopmental explanation correlating in utero exposure to adult-onset disease. Evidence of delayed disease development secondary to gestational exposure to naturally occurring DA has broad implications for marine mammal medicine and public health.

There are an estimated 5.4 million snakebite cases every year. People with snakebite envenoming suffer from severe complications, or even death. Although some review articles cover several topics of snakebite envenoming, a review of the cases regarding cerebral complications, especially rare syndromes, is lacking. Here, we overview 35 cases of snakebite by front-fanged snakes, including Bothrops, Daboia, Cerastes, Deinagkistrodon, Trimeresurus, and Crotalus in the Viperidae family; Bungarus and Naja in the Elapidae family, and Homoroselaps (rare cases) in the Lamprophiidae family. We also review three rare cases of snakebite by rear-fanged snakes, including Oxybelis and Leptodeira in the Colubridae family. In the cases of viper bites, most patients (17/24) were diagnosed with ischemic stroke and intracranial hemorrhage, leading to six deaths. We then discuss the potential underlying molecular mechanisms that cause these complications. In cases of elapid bites, neural, cardiac, and ophthalmic disorders are the main complications. Due to the small amount of venom injection and the inability to deep bite, all the rear-fanged snakebites did not develop any severe complications. To date, antivenom (AV) is the most effective therapy for snakebite envenoming. In the six cases of viper and elapid bites that did not receive AV, three cases (two by viper and one by elapid) resulted in death. This indicates that AV treatment is the key to survival after a venomous snakebite. Lastly, we also discuss several studies of therapeutic agents against snakebite-envenoming-induced complications, which could be potential adjuvants along with AV treatment. This article organizes the diagnosis of hemotoxic and neurotoxic envenoming, which may help ER doctors determine the treatment for unidentified snakebite.

Botulism is a neuroparalytic disease caused by a neurotoxin produced by Clostridium botulinum. This study aimed to genetically characterize C. botulinum strain isolated from the first case of infant botulism in Korea reported on June 17, 2019. We isolated C. botulinum strain CB-27 from a stool sample of the patient and analyzed the toxin types and toxin gene cluster compositions of the strain using a mouse bioassay, real-time PCR, and genome sequencing. Toxin gene cluster analysis showed that strain CB-27 possesses a C. botulinum neurotoxin type A harboring an unexpressed B gene. Although the nucleotide and amino acid sequences of toxin genes as well as the toxin gene cluster arrangements in strain CB-27 were identical to those of the known strain CDC_69094, the total nucleotide sequences of the toxin gene clusters of CB-27 differed from those of CDC_69094 by 0.47%, indicating genetic diversity of toxin gene clusters of CB-27 among other previously reported C. botulinum strains. To our knowledge, this is the first description of a C. botulinum strain with two separate toxin gene clusters in Korea.

BACKGROUND: Botulism is a rare syndrome resulting from the action of a neurotoxin produced by Clostridium botulinum, that it is potentially life threatening if diagnosis is delayed.
METHODS: We report a 26-year-old woman who presented an acute onset of bilateral cranial neuropathies associated with an anticholinergic syndrome in the absence fever leading to consider and confirm the diagnosis of botulism. At the end of follow-up, 7 weeks later, the outcome was favorable with an almost complete neurologic recovery.
CONCLUSIONS: Although botulism is uncommon, better awareness of its manifestations and high clinical suspicion should shorten diagnostic delay that makes the use of specific antitoxin ineffective. An acute onset of a bilateral oculomotor palsy, a fixed pupillary dilation and descending weakness in the absence of fever is typical of botulism. Outcome is usually favorable with a slow but full neurological recovery.

BACKGROUND: Ciguatera poisoning is one of the most prevalent types of fish poisoning, but it is often underreported, leading many health practitioners to be unfamiliar in correctly identifying and treating this toxicity.
METHODS: We present a case of ciguatera toxicity encountered in an emergency department in a Midwest community hospital setting. A 56-year-old woman presented to the ED with symptoms of perioral numbness, generalized pruritis, and hot/cold temperature reversal. Through careful history taking it was determined that the patient had recently returned from vacationing in the Caribbean and had been consuming meals containing various types of fish. A clinical diagnosis of ciguatera toxicity was made, and the patient was treated supportively. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: This topic is important in the realm of emergency medicine because it presents a known toxicologic pathogen in an unsuspecting geographic location. This case highlights the importance of maintaining broad differentials and considering a patient\'s travel and exposure history to make the clinical diagnosis of ciguatoxin as well as the importance of preventative management to avoid recurrence of symptoms. We review the etiology of this fascinating toxin as well as the clinical implications in the diagnosis and management of this toxicity.

The aim of this paper is to highlight the symptomatology in three Conium maculatum intoxication incidents, one of which was fatal. A number of studies were reviewed in order to update and summarize the relevant literature on the incidence, sociodemographic variables, method of poisoning, pathophysiology, diagnosis, variables associated with survival and fatality, management, and treatment of C. maculatum intoxication as well as the biosynthesis and biological effects of poison hemlock alkaloids. Results show that hemlock poisoning is relatively rare, although incidence varies in different regions, despite its worldwide distribution. Hemlock poisoning is more common in European and especially Mediterranean countries. The majority of the patients are adult males over 38 years of age. The clinical course of hemlock poisoning includes neurotoxicosis, tremor, vomiting, muscle paralysis, respiratory paralysis/failure, rhabdomyolysis, and acute renal failure. The therapeutic management focuses on absorption reduction, close observation for complications, and supportive therapy (especially for respiration). Acute occurrence is severe and life-threatening, but the survival rate is high if treatment is provided promptly. Recovery is rapid, generally taking only a few days.

In this article, a case of severe foodborne botulism in a 78-year-old man due to homemade pesto is presented. His initial symptoms were gastrointestinal problems. Later he suffered of cranial nerve palsies, muscle weakness of the upper extremities and respiratory failure, so he had to be admitted to the intensive care unit for mechanical ventilation. The botulism was confirmed by serology and culture. Because of spontaneously improving neurological deficits, we decided not to treat with the botulism antitoxin and the patient had complete clinical remission.

Scorpion α-toxins are polypeptides that inhibit voltage-gated sodium channel inactivation. They are divided into mammal, insect and α-like toxins based on their relative activity toward different phyla. Several factors are currently known to influence the selectivity, which are not just particular amino acid residues but also general physical, chemical, and topological properties of toxin structural modules. The objective of this study was to change the selectivity profile of a chosen broadly active α-like toxin, BeM9 from Mesobuthus eupeus, toward mammal-selective. Based on the available information on what determines scorpion α-toxin selectivity, we designed and produced msBeM9, a BeM9 derivative, which was verified to be exclusively active toward mammalian sodium channels and, most importantly, toward the Nav 1.2 isoform expressed in the brain.