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At least 55 records · Page 3Linked to original sources
USGS2015

Infectious diseases, parasites, and biological toxins in sea ducks

This chapter addresses disease agents in the broad sense, including viruses, bacteria, fungi, protozoan and helminth parasites, and biological toxins. Some of these agents are known to cause mortality in sea ducks, some are thought to be incidental findings, and the significance of others is yet poorly understood. Although the focus of the chapter is on free-living sea ducks, the study of disease in this taxonomic group has been relatively limited and examples from captive sea ducks and other wild waterfowl are used to illustrate the pathogenicity of certain diseases. Much of the early work in sea ducks consisted of anecdotal and descriptive reports of parasites, but it was soon recognized that diseases such as avian cholera, renal coccidiosis, and intestinal infections with acanthocephalans were causes of mortality in wild populations. More recently, adenoviruses, reoviruses, and the newly emergent Wellfleet Bay virus, for example, also have been linked to die-offs of sea ducks. Declining populations of animals are particularly vulnerable to the threats posed by disease and it is important that we improve our understanding of the significance of disease in sea ducks. To conclude, we offer our recommendations for future directions in this field.

Book chapter↗
USGS1938

The distribution of botulinus toxin in duck sickness areas

One of the most important events in the history of the diseases of wildfowl wa the discovery of the cause of western duck sickness. Determination that this malady of migratory birds is not a chemical poisoning, as had been previously suspected, was made by Kalmbach and others in 1930-31. Thtat it is a food poisoning resulting from toxins produced by botulinus organisms was proved beyond question. An extensive review of the work leading up to this determination cannot be made in this paper, but some orientation is necessary to a proper appreciation of the subject.

Conference Paper↗
USGS2025

Diel and spatial variability in cyanobacterial composition, gene abundance, and toxin concentration: A pilot study

We designed a pilot field study to assess relations between sunlight, cyanobacteria, and cyanotoxins. In 2021, we collected day (07:00 h, 10:00 h, 13:00 h, 16:00 h) and night samples (19:00 h, 22:00 h, 01:00 h, 04:00 h) at two locations in Kabetogama Lake, MN, USA. One sample set was collected from the lakeward end of a boat dock and the other on the nearby shoreline. Cyanobacterial phylogenetic eDNA differences over 24 h (pseudo F = 2.0938, p = 0.127) were not significant. Copies of anatoxin ( anaC ) and microcystin ( mcyE ) synthetase genes varied significantly over the sampling times at the dock (Friedman Χ 2 = 15.01, df = 7, p = 0.036; Friedman Χ 2 = 19.22, df = 7, p = 0.008) and the shoreline (Friedman Χ 2 = 19.33, df = 7, p = 0.007; Friedman Χ 2 = 20.56, df = 7, p = 0.005), with the highest anaC counts occurring during the night for both sites. Additionally, the highest total and dissolved microcystin concentrations occurred at night. Despite the proximity of the sampling locations, cyanobacterial phylogenetic eDNA results indicate that the variability between sites (pseudo-F = 27.547, p = 0.001) were greater than temporal differences over 24 h (pseudo F = 2.0938, p = 0.127). Understanding the effect of diel and spatial variability may help researchers and resource managers make informed decisions about sampling and potential exposure.

Minnesota↗
USGS2015

A plant toxin mediated mechanism for the lag in snowshoe hare population recovery following cyclic declines

A necessary condition for a snowshoe hare population to cycle is reduced reproduction after the population declines. But the cause of a cyclic snowshoe hare population's reduced reproduction during the low phase of the cycle, when predator density collapses, is not completely understood. We propose that moderate-severe browsing by snowshoe hares upon preferred winter-foods could increase the toxicity of some of the hare's best winter-foods during the following hare low, with the result being a decline in hare nutrition that could reduce hare reproduction. We used a combination of modeling and experiments to explore this hypothesis. Using the shrub birch Betula glandulosa as the plant of interest, the model predicted that browsing by hares during a hare cycle peak, by increasing the toxicity B. glandulosa twigs during the following hare low, could cause a hare population to cycle. The model's assumptions were verified with assays of dammarane triterpenes in segments of B. glandulosa twigs and captive hare feeding experiments conducted in Alaska during February and March 1986. The model's predictions were tested with estimates of hare density and measurements of B. glandulosa twig growth made at Kluane, Yukon from 1988–2008. The empirical tests supported the model's predictions. Thus, we have concluded that a browsing-caused increase in twig toxicity that occurs during the hare cycle's low phase could reduce hare reproduction during the low phase of the hare cycle.

Yukon↗
USGS2023

Native amphibian toxin reduces invasive crayfish feeding with potential benefits to stream biodiversity

Background Biodiversity is generally reduced when non-native species invade an ecosystem. Invasive crayfish, Procambarus clarkii , populate California freshwater streams, and in the Santa Monica Mountains (Los Angeles, USA), their introduction has led to trophic cascades due to omnivorous feeding behavior and a rapid rate of population growth. The native California newt, Taricha torosa , possesses a neurotoxin, tetrodotoxin (TTX), that affects freshwater animal behavior. Given P. clarkii has a limited evolutionary history with TTX, we hypothesized that TTX may affect crayfish feeding behaviors. To determine if TTX affects P. clarkii behavior, we measured cumulative movement and various feeding behaviors of P. clarkii exposed to (i) waterborne, ecologically realistic concentrations of TTX (~ 3.0 × 10 − 8 moles/L), (ii) an anuran chemical cue to account for intraguild cues, or (iii) a T. torosa chemical cue with quantitated TTX in it (~ 6.2 × 10 − 8 moles/L). Results We found that the presence of TTX in any form significantly reduced crayfish movement and decreased the amount of food consumed over time. Crayfish responses to the anuran treatment did not significantly differ from controls. Conclusion Our laboratory results show that naturally occurring neurotoxin from native California newts limits invasive crayfish foraging and feeding rates, which may play a role in preserving local stream ecosystems by limiting invasive crayfish behaviors that are detrimental to biodiversity.

California↗
USGS2018

Nitrogen limitation, toxin synthesis potential, and toxicity of cyanobacterial populations in Lake Okeechobee and the St. Lucie River Estuary, Florida, during the 2016 state of emergency event

Lake Okeechobee, FL, USA, has been subjected to intensifying cyanobacterial blooms that can spread to the adjacent St. Lucie River and Estuary via natural and anthropogenically-induced flooding events. In July 2016, a large, toxic cyanobacterial bloom occurred in Lake Okeechobee and throughout the St. Lucie River and Estuary, leading Florida to declare a state of emergency. This study reports on measurements and nutrient amendment experiments performed in this freshwater-estuarine ecosystem (salinity 0–25 PSU) during and after the bloom. In July, all sites along the bloom exhibited dissolved inorganic nitrogen-to-phosphorus ratios < 6, while Microcystis dominated (> 95%) phytoplankton inventories from the lake to the central part of the estuary. Chlorophyll a and microcystin concentrations peaked (100 and 34 μg L -1 , respectively) within Lake Okeechobee and decreased eastwards. Metagenomic analyses indicated that genes associated with the production of microcystin ( mcyE ) and the algal neurotoxin saxitoxin ( sxtA ) originated from Microcystis and multiple diazotrophic genera, respectively. There were highly significant correlations between levels of total nitrogen, microcystin, and microcystin synthesis gene abundance across all surveyed sites ( p < 0.001), suggesting high levels of nitrogen supported the production of microcystin during this event. Consistent with this, experiments performed with low salinity water from the St. Lucie River during the event indicated that algal biomass was nitrogen-limited. In the fall, densities of Microcystis and concentrations of microcystin were significantly lower, green algae co-dominated with cyanobacteria, and multiple algal groups displayed nitrogen-limitation. These results indicate that monitoring and regulatory strategies in Lake Okeechobee and the St. Lucie River and Estuary should consider managing loads of nitrogen to control future algal and microcystin-producing cyanobacterial blooms.

Florida↗
USGS2010

Algal toxins in Upper Klamath Lake, Oregon: Linking water quality to juvenile sucker health

As the lead science agency for the Department of Interior, the U.S. Geological Survey is actively involved in resource issues in the Klamath River basin. Activities include research projects on endangered Lost River and shortnose suckers, threatened coho salmon, groundwater resources, seasonal runoff forecasting, water quality in Upper Klamath Lake and the Klamath River, nutrient cycling in wetlands, and assessment of land idling programs to reduce water consumption. Many of these studies are collaborations with various partners including Department of Interior agencies, Indian Tribes, and State agencies.

Oregon↗
USGS2013

Initial results from a reconnaissance of cyanobacteria and associated toxins in Illinois, August--October 2012

Ten lakes and two rivers in Illinois were sampled in August–October 2012 to determine the concentrations and spatial distribution of cyanobacteria and associated cyanotoxins throughout the State. The reconnaissance was a collaborative effort of the U.S. Geological Survey and the Illinois Environmental Protection Agency. Sample results indicated that concentrations of both total cyanobacterial cells and microcystin were commonly at levels likely to result in adverse human health effects, according to World Health Organization guidance values. Concentrations generally decreased from August to October following precipitation events and lower temperatures.

Illinois↗
USGS1994

Waterfowl botulism--a brief summary

Botulism is a food poisoning caused by the ingestion of the toxin produced by the bacterium Clostridium botulinum of any of six strains, designated A through F. The disease, as it occurs in epidemic proportion in wild birds, is most commonly of the C type, although outbreaks caused by type E botulism have been observed on the Great Lakes. C. botulinum is a widely distributed anaerobic bacterium which is capable of existence for many years in spore form. Its vegetative cells grow and synthesize toxin, whenever and wherever the proper conditions exist in their environment. Outbreaks of botulism occur when aquatic birds consume this toxin which has been preformed in their food. Botulism is, therefore, an intoxication rather than an infection and is not a contagious disease. Botulism can be diagnosed conclusively only by demonstration of the toxin in the blood or serum of live affected birds, and a diagnostic laboratory should be contacted to confirm field diagnoses. A conclusive diagnosis cannot be reached by demonstrating the toxin or the organism in dead animals. The 'microenvironment concept' assumes that C. botulinum produces toxin in small, discrete, particulate food items which provide the requirements for growth of the bacteria independent of the surrounding wetland environment and which protect the toxin from dilution or inactivation. Optimum conditions for C. botulinum growth and toxin production include the absence of oxygen, a temperature of 76 deg. to 98 deg. F and suitable organic media, especially those composed of animal protein. Such conditions may be met in decaying invertebrate carcasses even though external conditions are unfavorable for toxin production. Vertebrate carcasses also may provide suitable conditions for the production of toxin, and maggots collected from duck carcasses during botulism outbreaks frequently contain extremely high levels of toxin. In determining the specific source of toxin and recommending control measures in the dynamic, complex, and diverse conditions of specific wetland ecosystem where botulism occurs, one's conclusions must necessarily become more speculative. Possibilities for reducing waterfowl losses due to botulism--Complete elimination of the causative organism, C. botulinum , from the wetland ecosystem is neither practical nor possible. Control methods may sometimes be profitably directed at prevention of toxin production, and the quantity of suitable media can be influenced. Rising water levels may drown terrestrial invertebrates, or flood vegetation thereby releasing nutrients which stimulate the increase in aquatic invertebrate populations to unstable levels which collapse. In other situations decreasing water levels may increase the numbers of invertebrate carcasses by increasing water temperatures or salinity which had been marginal for survival of previously thriving invertebrate populations or by stranding invertebrates on mud flats subject to periodic wind flooding. Therefore, a basic and important step in controlling botulism is stabilization of the wetland ecosystem in order to avoid the accumulation of decaying animal protein, especially during periods when temperatures are favorable for toxin production in these media. This can sometimes be accomplished by water level manipulation. If toxin production cannot be controlled by reducing the quantity of suitable media, another step is to prevent the ingestion of the toxic food items. Birds may be chased or lured from areas of toxin source or areas can be made less attractive by rapid and complete drainage, or draw down to a stable shoreline, where wind flooding does not occur. Removal of vertebrate carcasses, especially those of birds dying during the outbreak, reduces the availability of toxic maggots but carcass removal must be carried out frequently and diligently.Prevention of the effects of the toxin can be accomplished in some instances. Some degree of active immunity can be produced by injections of specific toxoi

Report↗
USGS2002

The epizootiology of type C botulism in fish-eating birds at Salton Sea, California

During 1996, type C avian botulism killed over 15,000 fish-eating birds at the Salton Sea in southern California. Amont those affected were nearly 10,000 western white pelicans (Pelecanus erythrorhynchos) and over 1,200 endangered California brown pelicans (Pelecanus occidentalis californicus). Since 1996, smaller epizootics have occurred every year. Type C botulism is not typically associated with fish-eating birds. In the case of the Salton Sea, Mozambique tilapia (Oreochromis mossambicus) are the suspected source of type C toxin, although the mechanism by which the fish acquire the toxin is still unknown. The goals of this study were to: 1) Determine presence/absence of active Clostridium botulinum type C and type C botulinum toxin in tilapia in the Salton Sea. 2) Use geospatial analyses to evaluate relationships between patterns of mortality in birds and fish and presence/absence of toxin and/or toxin-producing bacteria in sediments and fish. We investigated a method of detecting C. botulinum type C cells in the intestinal contents of Mozambique tilapia. This method involved extraction of predominantly cellular DNA and uses a polymerase chain reaction assay to detect presence of type C toxin gene. We collected sick, dead and healthy fish from various sites throughout the Sea during the summers of 1999 to 2001 in order to test them for the presence of active C. botulinum type C by PCR and for the presence of type C toxin by ELISA and mouse test. The results demonstrate that the tilapia population in the Salton Sea harbors C. botulinum type C cells within their gastrointestinal tract and the prevalence of this organism varies from year to year. The total number of fish with toxin-producing bacteria was significantly greater in 2000 than in 2001. No difference in the numbers of positives was detected between sick and dead fish compared to live fish, and there were no differences noted with regard to location of fish collection. The prevalence of active type C toxin in tilapia was low and the majority of samples positive for toxin by ELISA were negative on mouse test. Further investigation is currently underway. From 1999-2001, routine surveillance was conducted July through November to detect morbidity and mortality in pelicans. Location of retrieval and total number of birds collected were documented. In all three years, the majority of botulism-affected pelicans were retrieved from the vicinities of the river deltas although the Whitewater River had the fewest birds of the three. It has yet to be determined what roles the tilapia and pelican populations play in influencing these patterns.

California↗
USGS2003

Determination of the median toxic dose of type C botulism in lactating dairy cows

Because of the difficulty in identifying botulinum toxin in cattle, it is hypothesized that cattle are sensitive to levels of toxin below the detection limits of current diagnostic techniques (the mouse protection bioassay and the immunostick enzyme-linked immunosorbent assay [ELISA] for type C botulinum toxin). Using an up-down method for toxicologic testing, the median toxic dose (MTD50) for cattle was determined. Four lactating Holstein cows were dosed at 0.125 or 0.25 ng/kg with Clostridium botulinum type C toxin and failed to develop clinical signs of botulism during the 7-day observation period. Three cows given 0.50 ng/kg of toxin developed clinical signs of botulism. From these results, the MTD50 was calculated at 0.388 ng/kg (3.88 mouse lethal doses/kg) using the trim-logit method. These results suggest that cattle are 12.88 times more sensitive to type C botulinum toxin than a mouse on a per kilogram weight basis. The mouse protection bioassay and the immunostick ELISA for type C botulinum toxin failed to identify the presence of the toxin in the serum, blood, and milk samples taken from all 7 animals.

Journal of Veterinary Diagnostic Investigation↗