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Tonie E. Rocke

Publications and source records attributed to Tonie E. Rocke.

At least 91 records · Page 5Linked to original sources
USGS2010

Enzootic plague reduces black-footed ferret (Mustela nigripes) survival in Montana

Black-footed ferrets ( Mustela nigripes ) require extensive prairie dog colonies ( Cynomys spp.) to provide habitat and prey. Epizootic plague kills both prairie dogs and ferrets and is a major factor limiting recovery of the highly endangered ferret. In addition to epizootics, we hypothesized that enzootic plague, that is, presence of disease-causing Yersinia pestis without any noticeable prairie dog die off, may also affect ferret survival. We reduced risk of plague on portions of two ferret reintroduction areas by conducting flea control for 3 years. Beginning in 2004, about half of the ferrets residing on dusted and nondusted colonies were vaccinated against plague with an experimental vaccine (F1-V fusion protein). We evaluated 6-month reencounter rates (percentage of animals observed at the end of an interval that were known alive at the beginning of the interval), an index to survival, for ferrets in four treatment groups involving all combinations of vaccination and flea control. For captive-reared ferrets (115 individuals observed across 156 time intervals), reencounter rates were higher for vaccinates (0.44) than for nonvaccinates (0.23, p  = 0.044) on colonies without flea control, but vaccination had no detectable effect on colonies with flea control (vaccinates = 0.41, nonvaccinates = 0.42, p  = 0.754). Flea control resulted in higher reencounter rates for nonvaccinates ( p  = 0.026), but not for vaccinates ( p  = 0.508). The enhancement of survival due to vaccination or flea control supports the hypothesis that enzootic plague reduces ferret survival, even when there was no noticeable decline in prairie dog abundance. The collective effects of vaccination and flea control compel a conclusion that fleas are required for maintenance, and probably transmission, of plague at enzootic levels. Other studies have demonstrated similar effects of flea control on several species of prairie dogs and, when combined with this study, suggest that the effects of enzootic plague are widespread. Finally, we demonstrated that the experimental F1-V fusion protein vaccine provides protection to ferrets in the wild.

Vector-Borne and Zoonotic Diseases↗
USGS2009

Comparison of monkeypox viruses pathogenesis in mice by in vivo imaging

Monkeypox viruses (MPXV) cause human monkeypox, a zoonotic smallpox-like disease endemic to Africa, and are of worldwide public health and biodefense concern. Using viruses from the Congo (MPXV-2003-Congo-358) and West African (MPXV-2003-USA-044) clades, we constructed recombinant viruses that express the luciferase gene (MPXV-Congo/Luc+and MPXV-USA-Luc+) and compared their viral infection in mice by biophotonic imaging. BALB/c mice became infected by both MPXV clades, but they recovered and cleared the infection within 10 days post-infection (PI). However, infection in severe combined immune deficient (SCID) BALB/c mice resulted in 100% lethality. Intraperitoneal (IP) injection of both MPXV-Congo and MPXV-Congo/Luc+resulted in a systemic clinical disease and the same mean time-to-death at 9 (??0) days post-infection. Likewise, IP injection of SCID-BALB/c mice with MPXV-USA or the MPXV-USA-Luc+, resulted in similar disease but longer (P<0.05) mean time-to-death (11??0 days) for both viruses compared to the Congo strains. Imaging studies in SCID mice showed luminescence in the abdomen within 24 hours PI with subsequent spread elsewhere. Animals infected with the MPXV-USA/Luc+had less intense luminescence in tissues than those inoculated with MPXV-Congo/Luc+, and systemic spread of the MPXV-USA/Luc+virus occurred approximately two days later than the MPXV-Congo/Luc+. The ovary was an important target for viral replication as evidenced by the high viral titers and immunohistochemistry. These studies demonstrate the suitability of a mouse model and biophotonic imaging to compare the disease progression and tissue tropism of MPX viruses.

PLoS ONE↗
USGS2009

Attempts to identify Clostridium botulinum toxin in milk from three experimentally intoxicated Holstein cows

Three adult lactating Holstein cows were injected in the subcutaneous abdominal vein with 175 ng/kg of body weight of Clostridium botulinum type C toxin (451 cow median toxic doses) to determine if this botulinum toxin crosses the blood–milk barrier. Whole blood (in sodium heparin) and clotted blood serum samples were taken at 0 min, 10 min, and 3, 6, 9, and 12 h postinoculation. Milk samples were taken at 0 min and at 3, 6, 9 and 12 h postinoculation. All samples were tested for the presence of the toxin using the mouse bioassay and immunostick ELISA test. The immunostick ELISA identified the toxin in whole blood and the mouse bioassay identified the toxin in serum at all times examined in all 3 animals. Toxin was not identified by either detection method in milk samples collected from the 3 animals. From these results, it appears that Clostridium botulinum type C toxin does not cross from the blood to the milk in detectable concentrations.

Journal of Dairy Science↗
USGS2008

Exposure of mallards (Anas platyrhynchos) to the hepatotoxic cyanobacterium Nodularia spumigena

Nodularin (NODLN) is a cyclic pentapeptide hepatotoxin produced by the cyanobacterium Nodularia spumigena, which forms extensive blooms during the summer in the Baltic Sea. Nodularin was detected in liver, muscle and/or feather samples of several common eiders (Somateria mollissima) from the Gulf of Finland (northern Baltic Sea) in 2002-2005. Published information on the adverse effects of NODLN in marine birds is scarce. The aim of this study was to evaluate the toxicity of NODLN, and determine the concentrations of NODLN in liver and muscle tissue in mallards (Anas platyrhynchos) exposed to N. spumigena. Mallards received a single or multiple exposure via oral gavage with an aqueous slurry containing toxic N. spumigena. Dosages ranged from 200 to 600 ??g NODLN per kg body weight (bw). There were minimal histopathological changes in liver tissue, and brain cholinesterase activity did not differ among treatment groups. Concentrations of NODLN measured by LC-MS in liver varied between approximately 3-120 ??g kg-1 dry weight (dw) and ducks receiving multiple exposures had significantly greater liver toxin levels than ducks receiving the two lowest single exposures. In muscle, NODLN concentrations were approximately 2-6 ??g kg-1 dw, but did not differ significantly among exposure groups. This is the first in vivo lab study examining the effects and bioaccumulation of NODLN from N. spumigena in birds. The mallards in this study were resistant to adverse effects and did not bioaccumulate substantial levels of NODLN at the doses given. ?? 2008 Taylor & Francis.

Gulf of Finland↗
USGS2008

Avian botulism

This chapter contains section titled: Introduction Synonyms History Distribution Host Range Etiology Epizootiology Clinical Signs Pathogenesis Pathology Diagnosis Immunity Public Health Concerns Domestic Animal Health Concerns Wildlife Population Impacts Treatment and Control Literature Cited

Book chapter↗
USGS2008

Prominent pancreatic endocrinopathy and altered control of food intake disrupt energy homeostasis in prion diseases

Prion diseases are fatal neurodegenerative diseases that can induce endocrinopathies. The basis of altered endocrine function in prion diseases is not well understood, and the purpose of this study was to investigate the spatiotemporal relationship between energy homeostasis and prion infection in hamsters inoculated with either the 139H strain of scrapie agent, which induces preclinical weight gain, or the HY strain of transmissible mink encephalopathy (TME), which induces clinical weight loss. Temporal changes in body weight, feed, and water intake were measured as well as both non-fasted and fasted concentrations of serum glucose, insulin, glucagon, ??-ketones, and leptin. In 139H scrapie-infected hamsters, polydipsia, hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia were found at preclinical stages and are consistent with an anabolic syndrome that has similarities to type II diabetes mellitus and/or metabolic syndrome X. In HY TME-infected hamsters, hypodipsia, hypersecretion of glucagon (in both non-fasted and fasted states), increased fasted ??-ketones, fasted hypoglycemia, and suppressed non-fasted leptin concentrations were found while feed intake was normal. These findings suggest a severe catabolic syndrome in HY TME infection mediated by chronic increases in glucagon secretion. In both models, alterations of pancreatic endocrine function were not associated with PrPSc deposition in the pancreas. The results indicate that prominent endocrinopathy underlies alterations in body weight, pancreatic endocrine function, and intake of food. The prion-induced alterations of energy homeostasis in 139H scrapie- or HY TME-infected hamsters could occur within areas of the hypothalamus that control food satiety and/or within autonomic centers that provide neural outflow to the pancreas. ?? 2008 Society for Endocrinology.

Journal of Endocrinology↗
USGS2008

Protecting Black-Footed Ferrets and Prairie Dogs against sylvatic plague

Scientists at the USGS National Wildlife Health Center (NWHC), in collaboration with colleagues at other federal agencies and the University of Wisconsin, are developing and testing vaccines that can be used to protect black-footed ferrets and prairie dogs against plague. The black-footed ferret is commonly regarded as the most endangered mammal in North America, and sylvatic plague is a major impediment to its recovery. The three prairie dog species (Gunnison's, black-tailed, and white-tailed prairie dogs), upon which the ferret depends for food and whose burrows they use for shelter, have been drastically reduced from historical levels, resulting in the near extinction of the ferret. All three species are considered 'at risk' and have been petitioned for listing as 'threatened' or 'endangered' by the U.S. Fish and Wildlife Service (FWS). Additionally, the Utah prairie dog is listed as threatened and the Mexican prairie dog is considered endangered in Mexico. Like the black-footed ferret, all five prairie dog species are highly susceptible to plague and regularly experience outbreaks with devastating losses. Controlling plague outbreaks in prairie dogs and ferrets is a vital concern for ongoing recovery programs and conservation efforts for both species.

Fact Sheet↗
USGS2008

Vaccination with F1-V fusion protein protects black-footed ferrets (Mustela nigripes) against plague upon oral challenge with Yersinia pestis

Previous studies have established that vaccination of black-footed ferrets ( Mustela nigripes ) with F1-V fusion protein by subcutaneous (SC) injection protects the animals against plague upon injection of the bacterium Yersinia pestis . This study demonstrates that the F1-V antigen can also protect ferrets against plague contracted via ingestion of a Y. pestis -infected mouse, a probable route for natural infection. Eight black-footed ferret kits were vaccinated with F1-V protein by SC injection at approximately 60 days-of-age. A booster vaccination was administered 3 mo later via SC injection. Four additional ferret kits received placebos. The animals were challenged 6 wk after the boost by feeding each one a Y. pestis -infected mouse. All eight vaccinates survived challenge, while the four controls succumbed to plague within 3 days after exposure. To determine the duration of antibody postvaccination, 18 additional black-footed ferret kits were vaccinated and boosted with F1-V by SC injection at 60 and 120 days-of-age. High titers to both F1 and V (mean reciprocal titers of 18,552 and 99,862, respectively) were found in all vaccinates up to 2 yr postvaccination, whereas seven control animals remained antibody negative throughout the same time period.

Journal of Wildlife Diseases↗
USGS2006

Vaccination as a potential means to prevent plague in black-footed ferrets: Progress and continuing challenges

This study was conducted to further assess the feasibility of vaccinating black-footed ferrets ( Mustela nigripes ) against plague (caused by the bacterium Yersinia pestis ). On days 0 and 28, 17 postreproductive ferrets were immunized by subcutaneous injection with a recombinant fusion protein containing F1 and V antigens from Y. pestis. Another 17 animals received a placebo by the same route. Two weeks after the second immunization, mean antibody titers to Y. pestis F1 and V antigens were measured and found to be significantly higher in vaccinates than their preimmunization values (P < 0.0001) and significantly higher than the control values (P < 0.0001). Six months postimmunization, 16 vaccinates and eight controls were challenged with approximately 8,000 colony forming units of virulent plague by subcutaneous inoculation. Eleven of 16 vaccinates (69 percent) survived with no ill effects whereas all eight control animals died within 3a??6 days. Two months later, the 11 surviving vaccinates were challenged again by ingestion of a plague-infected mouse. None of the animals showed any ill effects and all survived. In contrast, seven control ferrets fed infected mice died within 2a??4 days, including one animal that did not actually ingest the mouse but was likely exposed to it. This study demonstrates that immunization of ferrets with the recombinant F1-V fusion protein can induce significant antibody responses and reduce their susceptibility to plague infection.

Scientific Investigations Report↗
USGS2005

Toxicoinfectious botulism in commercial caponized chickens

During the summer of 2003, two flocks of commercial broiler chickens experienced unusually high death losses following caponizing at 3 wk of age and again between 8 and 14 wk of age. In September, fifteen 11-wk-old live capons were submitted to the Iowa State University Veterinary Diagnostic Laboratory for assistance. In both flocks, the second episode of elevated mortality was associated with incoordination, flaccid paralysis of leg, wing, and neck muscles, a recumbent body posture characterized by neck extension, and diarrhea. No macroscopic or microscopic lesions were detected in affected chickens. Hearts containing clotted blood and ceca were submitted to the National Wildlife Health Center in Madison, WI. Type C botulinum toxin was identified in heart blood and ceca by mouse bioassay tests. Enzyme-linked immunosorbent assay tests on heart blood samples were also positive for type C botulinum toxin. Clostridium botulinum was isolated from the ceca and genes encoding type C botulinum toxin were detected in cecal contents by a polymerase chain reaction test. Chickens are less susceptible to botulism as they age, and this disease has not previously been documented in broilers as old as 14 wk of age. Wound contamination by spores of C. botulinum may have contributed to the unusually high death losses following caponizing.

Avian Diseases↗
USGS2005

Attempts to identify the source of avian vacuolar myelinopathy for waterbirds

Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots ( Fulica americana ), mallard ducks and ducklings ( Anas platyrhynchos ), quail ( Coturnix japonica ), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels ( Falco sparverius ), and American crows ( Corvus brachyrhynchos ). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla , or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.

Journal of Wildlife Diseases↗
USGS2004

Could blackbird mortality from avicide DRC-1339 contribute to avian botulism outbreaks in North Dakota?

Blackbird (family lcteridae) depredation on sunflower (Helianthus annuus) crops in the prairie states of the United States has motivated the proposed use of an avicide, DRC-1339 (3-chloro-4-methylaniline), to decrease their numbers. The resulting mortality of blackbirds at wetland roosts could increase the potential of avian botulism occurring in affected marshes. To assess this possibility, we seeded (artificially placed) blackbird carcasses in selected wetlands in Stutsman County, North Dakota, during August-September 2000 and July-September 2001 to evaluate their rate of decomposition and role in initiating avian botulism outbreaks. We monitored carcasses to determine their persistence, the frequency and amount of maggots produced, and the presence of type C botulinum toxin. In 10 of our 12 study wetlands, blackbird carcasses were not rapidly removed by scavengers, thus providing substrate for maggot growth and potential production of Clostridium botulinum toxin. Decomposition of carcasses occurred rapidly, and maggot production averaged 4a??5 g per carcass within 9 days. We were unable to detect C. botulinum type C toxin in any of the 377 blackbird carcasses or the 112 samples of maggots we collected in 2000 or 2001. None of the 25 blackbird carcasses we tested contained botulinum spores, the most probable explanation for the absence of botulinum toxin production. Our results indicate that the likelihood of DRC-1339-poisoned blackbirds causing botulism outbreaks would be minimal in North Dakota wetlands during late summer and early autumn.

North Dakota, South Dakota↗
USGS2004

Detection of Clostridium botulinum type C cells in the gastrointestinal tracts of Mozambique tilapia (Oreochromis mossambicus) by polymerase chain reaction

We established a method of directly detecting Clostridium botulinum type C cells, while minimizing spore detection, in the intestinal contents of Mozambique tilapia ( Oreochromis mossambicus ). This technique involved extraction of predominantly cellular DNA from tilapia intestinal tracts and used a polymerase chain reaction assay to detect presence of type C 1 toxin gene. We consistently detected C. botulinum type C cells in tilapia gastrointestinal contents at a level of 7.5×10 4 cells per 0.25 g material or 1.9×10 3 cells. This technique is useful for determining prevalence of the potentially active organisms within a given population of fish and may be adapted to other types of C. botulinum and vertebrate populations as well.

California↗
USGS2004

Type C botulism in pelicans and other fish-eating birds at the Salton Sea

In 1996, type C avian botulism killed over 10,000 pelicans and nearly 10,000 other fish-eating birds at the Salton Sea in southern California. Although botulism had been previously documented in waterbirds at the Sea, this die-off was unusual in that it involved primarily fish-eating birds. The American White Pelican ( Pelecanus erythrorynchos ) was the species with the greatest mortality in 1996. Since 1996, mortality has recurred every year but losses have declined (<2,000 birds/year), with relatively more Brown Pelicans ( P. occidentalis ) than White Pelicans afflicted. In 2000, morbidity and mortality of Brown Pelicans with type C botulism (1311) approached the numbers afflicted in 1996 (2034). In recent years, mortality reached a peak earlier in the summer, July and August, in contrast to 1996 when mortality reached a peak in September. An exotic fish species, tilapia ( Oreochromis mossambicus ), has been implicated as the source of toxin for birds at Salton Sea, but the source of toxin for fish is unknown.

California↗
USGS2004

Investigations of a large scale eared grebe (Podiceps nigricollis) die-off at the Salton Sea, California in 1992

An estimated 150,000 Eared Grebes (Podiceps nigricollis) died at the Salton Sea between 16 December 1991 and 21 April 1992. This represented the largest documented mortality event of Eared Grebes at the time and approximately 6% of the North American population. During the die-off, grebes exhibited several uncharacteristic behaviors, such as congregating at freshwater tributaries, repeatedly gulping freshwater, preening excessively, moving onto land, and allowing close approach and/or capture. Avian cholera was diagnosed in Eared Grebes collected along the north and west shoreline of the Sea late in the die-off but not from the majority of the Eared Grebes dying along the south shore. Gross and histological examinations and diagnostic testing for viruses, bacteria, and parasites did not identify the cause of mortality in the majority of Eared Grebes examined from the south shore of the Sea. Liver concentrations of arsenic, chromium, DDE, mercury, selenium, and zinc were elevated in some Eared Grebes, but none of those contaminants exceeded known thresholds for independent lethality. Poisoning by heavy metals, organochlorine, organophosphorus, or carbamate pesticides, avian botulism, and salt were ruled out as the cause of mortality. Hypotheses for the die-off are interactive effects of contaminants, immunosuppression, a yet unidentified biotoxin or pathogen present in the Salton Sea, impairment of feather waterproofing leading to hypothermia, or a unique manifestation of avian cholera that evades laboratory detection.

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↗
USGS2003

Recombinant raccoon pox vaccine protects mice against lethal plague

Using a raccoon poxvirus (RCN) expression system, we have developed new recombinant vaccines that can protect mice against lethal plague infection. We tested the effects of a translation enhancer (EMCV-IRES) in combination with a secretory (tPA) signal or secretory (tPA) and membrane anchoring (CHV-gG) signals on in vitro antigen expression of F1 antigen in tissue culture and the induction of antibody responses and protection against Yersinia pestis challenge in mice. The RCN vector successfully expressed the F1 protein of Y. pestis in vitro. In addition, the level of expression was increased by the insertion of the EMCV-IRES and combinations of this and the secretory signal or secretory and anchoring signals. These recombinant viruses generated protective immune responses that resulted in survival of 80% of vaccinated mice upon challenge with Y. pestis . Of the RCN-based vaccines we tested, the RCN-IRES-tPA-YpF1 recombinant construct was the most efficacious. Mice vaccinated with this construct withstood challenge with as many as 1.5 million colony forming units of Y. pestis (7.7×10 4 LD 50 ). Interestingly, vaccination with F1 fused to the anchoring signal (RCN-IRES-tPA-YpF1-gG) elicited significant anti-F1 antibody titers, but failed to protect mice from plague challenge. Our studies demonstrate, in vitro and in vivo, the potential importance of the EMCV-IRES and secretory signals in vaccine design. These molecular tools provide a new approach for improving the efficacy of vaccines. In addition, these novel recombinant vaccines could have human, veterinary, and wildlife applications in the prevention of plague.

Vaccine↗