Paralytic and Amnesic Shellfish Toxins Impacts on Seabirds, Analyses and Management.

Marine biotoxins have been frequently implicated in morbidity and mortality events in numerous species of birds worldwide. Nevertheless, their effects on seabirds have often been overlooked and the associated ecological impact has not been extensively studied. On top of that, the number of published studies confirming by analyses the presence of marine biotoxins from harmful algal blooms (HABs) in seabirds, although having increased in recent years, is still quite low. This review compiles information on studies evidencing the impact of HAB toxins on marine birds, with a special focus on the effects of paralytic and amnesic shellfish toxins (PSTs and ASTs). It is mainly centered on studies in which the presence of PSTs and/or ASTs in seabird samples was demonstrated through analyses. The analytical techniques commonly employed, the tissues selected and the adjustments done in protocols for processing seabird matrixes are summarized. Other topics covered include the role of different vectors in the seabird intoxications, information on clinical signs in birds affected by PSTs and ASTs, and multifactorial causes which could aggravate the syndromes. Close collaboration between seabird experts and marine biotoxins researchers is needed to identify and report the potential involvement of HABs and their toxins in the mortality events. Future studies on the PSTs and ASTs pharmacodynamics, together with the establishment of lethal doses in various seabird species, are also necessary. These studies would aid in the selection of the target organs for toxins analyses and in the postmortem intoxication diagnoses.

Paralytic shellfish poisoning and palytoxin poisoning in dogs.

BACKGROUND: Fatal cases of exposure to paralytic shellfish toxins and palytoxins have occurred in companion animals but are poorly described. METHODS: We describe one case of paralytic shellfish poisoning (PSP) and three cases of palytoxin poisoning in dogs. RESULTS: Mild PSP occurred following ingestion of crab while walking on a beach. Analysis confirmed the presence of paralytic shellfish toxins, particularly decarbamoyl saxitoxin, in clinical samples and marine organisms. This case occurred shortly after an outbreak of PSP in dogs on the eastern coast of England. Palytoxin poisoning occurred in a dog after it chewed coral removed from an aquarium. Signs included collapse, hypothermia, bloody diarrhoea and respiratory distress. The dog was euthanised due to rapid deterioration and poor prognosis. Palytoxin was not detected in a premortem blood sample. Two other dogs in a separate incident developed only mild signs (fever and respiratory distress) after suspected exposure to aerosolised palytoxin and recovered within a few hours. CONCLUSION: Cases of PSP are episodic and not common in dogs. Cases of palytoxin exposure are reportedly increasing in humans, and there is presumably also an increased risk to pets. There is no specific treatment for PSP or palytoxin poisoning.

Fatal Canine Intoxications Linked to the Presence of Saxitoxins in Stranded Marine Organisms Following Winter Storm Activity.

At the start of 2018, multiple incidents of dog illnesses were reported following consumption of marine species washed up onto the beaches of eastern England after winter storms. Over a two-week period, nine confirmed illnesses including two canine deaths were recorded. Symptoms in the affected dogs included sickness, loss of motor control, and muscle paralysis. Samples of flatfish, starfish, and crab from the beaches in the affected areas were analysed for a suite of naturally occurring marine neurotoxins of dinoflagellate origin. Toxins causing paralytic shellfish poisoning (PSP) were detected and quantified using two independent chemical testing methods in samples of all three marine types, with concentrations over 14,000 µg saxitoxin (STX) eq/kg found in one starfish sample. Further evidence for PSP intoxication of the dogs was obtained with the positive identification of PSP toxins in a vomited crab sample from one deceased dog and in gastrointestinal samples collected post mortem from a second affected dog. Together, this is the first report providing evidence of starfish being implicated in a PSP intoxication case and the first report of PSP in canines.

The role of a PSP-producing Alexandrium bloom in an unprecedented diamondback terrapin (Malaclemys terrapin) mortality event in Flanders Bay, New York, USA.

Diamondback terrapins (Malaclemys terrapin) are a threatened or endangered species in much of their range along the U.S. Atlantic and Gulf coasts. Over an approximately three-week period from late April to mid-May 2015, hundreds of adult diamondback terrapins were found dead on the shores of Flanders Bay, Long Island, New York, USA. Concurrent with the mortality event, elevated densities of the paralytic shellfish toxin (PST)-producing dinoflagellate, Alexandrium fundyense (>104 cells L-1) and high levels of PST in bivalves (maximal levels = 540 µg STX eq. 100 g-1 shellfish tissue) were observed in the Flanders Bay region, resulting in shellfish bed closures in regional tributaries. Gross and histologic postmortem examinations of terrapins revealed no physical trauma to individuals or a common, underlying disease process to explain the deaths. PST compounds (0.2-12.5 µg STX eq. 100 g-1) were present in various M. terrapin tissues collected over the duration of the mortality event. High-throughput sequencing revealed that the ribbed mussel (Geukensia demissa, a PST vector) was present in the gastrointestinal tracks of all terrapin samples tested. While the potential of PST to cause mortality in chelonians has not been well-characterized, in the absence of other significant findings from necropsies and pathological analyses, we provide evidence that PST in shellfish was likely high enough to cause or contribute to the mortality in these small (<2.0 kg) animals.

Fatal paralytic shellfish poisoning in Kittlitz's Murrelet (Brachyramphus brevirostris) nestlings, Alaska, USA.

Paralytic shellfish poisoning (PSP) is an acute toxic illness in humans resulting from ingestion of shellfish contaminated with a suite of neurotoxins (saxitoxins) produced by marine dinoflagellates, most commonly in the genus Alexandrium. Poisoning also has been sporadically suspected and, less often, documented in marine wildlife, often in association with an outbreak in humans. Kittlitz's Murrelet (Brachyramphus brevirostris) is a small, rare seabird of the Northern Pacific with a declining population. From 2008 to 2012, as part of a breeding ecology study, multiple Kittlitz's Murrelet nests on Kodiak Island, Alaska, were monitored by remote cameras. During the 2011 and 2012 breeding seasons, nestlings from several sites died during mild weather conditions. Remote camera observations revealed that the nestlings died shortly after consuming sand lance (Ammodytes hexapterus), a fish species known to biomagnify saxitoxin. High levels of saxitoxin were subsequently documented in crop content in 87% of nestling carcasses. Marine bird deaths from PSP may be underreported.

Domoic acid epileptic disease.

Domoic acid epileptic disease is characterized by spontaneous recurrent seizures weeks to months after domoic acid exposure. The potential for this disease was first recognized in a human case study of temporal lobe epilepsy after the 1987 amnesic shellfish-poisoning event in Quebec, and was characterized as a chronic epileptic syndrome in California sea lions through investigation of a series of domoic acid poisoning cases between 1998 and 2006. The sea lion study provided a breadth of insight into clinical presentations, unusual behaviors, brain pathology, and epidemiology. A rat model that replicates key observations of the chronic epileptic syndrome in sea lions has been applied to identify the progression of the epileptic disease state, its relationship to behavioral manifestations, and to define the neural systems involved in these behavioral disorders. Here, we present the concept of domoic acid epileptic disease as a delayed manifestation of domoic acid poisoning and review the state of knowledge for this disease state in affected humans and sea lions. We discuss causative mechanisms and neural underpinnings of disease maturation revealed by the rat model to present the concept for olfactory origin of an epileptic disease; triggered in dendodendritic synapases of the olfactory bulb and maturing in the olfactory cortex. We conclude with updated information on populations at risk, medical diagnosis, treatment, and prognosis.