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At least 739 records · Page 41Linked to original sources

Overview of recent DNA vaccine development for fish

Since the first description of DNA vaccines for fish in 1996, numerous studies of genetic immunisation against the rhabdovirus pathogens infectious haematopoietic necrosis virus (IHNV) and viral haemorrhagic septicaemia virus (VHSV) have established their potential as both highly efficacious biologicals and useful basic research tools. Single small doses of rhabdovirus DNA constructs provide extremely strong protection against severe viral challenge under a variety of conditions. DNA vaccines for several other important fish viruses, bacteria, and parasites are under investigation, but they have not yet shown high efficacy. Therefore, current research is focussed on mechanistic studies to understand the basis of protection, and on improvement of the nucleic acid vaccine applications against a wider range of fish pathogens.

Conference Paper↗

Dealing with largemouth bass virus: benefits of multisector collaboration

Largemouth bass virus (LMBV), a recently identified pathogen, affected largemouth bass (Micropterus salmoides) in the southeastern United States beginning in the 1990s. Concern about the impacts of this little-known pathogen on largemouth bass populations, effects on fisheries management, and the need to provide anglers and the media with consistent and accurate information prompted a private organization (Bass Anglers Sportsman Society) to invite managers and researchers from state and federal agencies and universities to a series of five annual public workshops beginning in 2000. These workshops provided a mechanism to share information, identify and prioritize action items, and develop consensus information and outreach materials that could be provided to bass anglers and the media. Regionalizing the LMBV issue and collaboration among researchers, managers, and a fishing organization may also have allayed angler and media concerns. The process embodied in these workshops is offered as a successful example of multi-agency, multi-sector collaboration to facilitate information acquisition and guide action to address a regional fisheries management issue.

Conference Paper↗

A baseline analysis of the distribution, host-range, and severity of the rust Puccinia Psidii in the Hawaiian islands, 2005-2010

Puccinia psidii was first described by Winter (1884) on guava ( Psidium guajava L.) in Brazil. The rust is still a major pest of native guava in Brazil and is often referred to as “guava rust” internationally. It is unusual among rust fungi because of its broad and ever-expanding host-range within the Myrtaceae plant family (Simpson et al . 2006). The pathogen is regarded as a major threat to Eucalyptus plantations and other Myrtaceae worldwide (Coutinho et al . 1998, Grgurinovic et al . 2006, Glen et al . 2007). Infections of leaves and meristems are particularly severe on susceptible seedlings, cuttings, young trees, and coppice, causing plants to be stunted and multi-branched, inhibiting normal growth and development, and sometimes causing death to young seedlings (Booth et al . 2000, Rayachhetry et al . 2001). The fungus has expanded its host-range in Brazil, affecting both native and introduced Myrtaceae (Coutinho et al . 1998). Since its discovery in 1884, P. psidii has continually been discovered to have an expanding host-range within the Myrtaceae, affecting hosts throughout much of South and Central America and the Caribbean. Spreading out originally from Brazil in 1884, the fungus has been reported on hosts in the following countries (first record in parentheses): Paraguay (1884), Uruguay (1889), Ecuador (1891), Colombia (1913), Puerto Rico (1913), Cuba (1926), Dominican Republic (1933), Venezuela (1934), Jamaica (1936), Argentina (1946), Dominica (1948), Trinidad and Tobago (1951), Guatemala (1968), United States (Florida; 1977), Mexico (1981), El Salvador (1987), and Costa Rica (1998) (Simpson et al . 2006). It is possible that P. psidii was present in El Salvador and Costa Rica prior to 1980, but was not reported until 1987 and 1998, respectively. Until recently, Puccinia psidii was restricted to the Neotropics, Mexico, and the state of Florida in the United States. While the rust has been present in Florida for over 30 years, only recently has it spread westward. Although possibly present earlier, P. psidii was found in California in November 2005 in a nursery in San Diego County on Myrtus communis and documented by a report in a nursery newsletter (Mellano 2006). Puccinia psidii was first found in Hawai`i on a young plant of `ōhi`a ( Metrosideros polymorpha ) in April 2005, in a nursery on the island of O`ahu (Killgore and Heu 2005; Uchida et al . 2006). The fungus subsequently spread to most islands of the Hawaiian chain, infecting `ōhi`a and other myrtaceous hosts (Hauff 2006, Anderson et al . 2007). P. psidii was first found in Japan in May 2007 on cultivated `ōhi`a (Kawanishi et al . 2009). Most recently, a rust identified as Uredo rangelii was discovered in April 2010 in New South Wales, Australia (Carnegie et al . 2010). This rust is closely related to Puccinia psidii and is part of the guava rust complex described by Simpson et al . (2006). Although treated as a separate species by Simpson et al. (2006), many authors now consider U. rangelii a synonym for U. psidii , which is the anamorph (asexual stage) of P. psidii , and therefore, the same species (Glen et al . 2007, Carnegie et al . 2010). Because of the large diversity of native Myrtaceae present in Australia, the number of Myrtaceae hosts attacked by species of the guava rust complex will likely grow now that U. rangelii has arrived and is spreading in the country. As of this writing (June 2011), 94 species of Myrtaceae have been identified as hosts of U. rangelii in the states of New South Wales and Queensland. Damage is severe on nearly one-third of the species affected, and 16 of these species are threatened or endangered native species (Secretary of Australia, May 2011). The presence of Puccinia psidii in Hawai`i is particularly alarming for at least two reasons: (1) M. polymorpha is the dominant overstory tree of the native forest, and (2) P. psidii is now established in the Pacific region, where numerous Myrtaceae species are native. Native ecosystems in Hawai`i and the Pacific could be seriously affected by the spread of P. psidii , as both native and introduced Myrtaceae are significant components of many different plant communities throughout the region (Glen et al. 2007). Because the guava rust complex (i.e., P. psidii and U. rangelii ) now attacks well over 100 species of Myrtaceae worldwide, it is currently a priority for international quarantine and import restrictions in an effort to prevent further spread among Australasian and Pacific Myrtaceae. Several different studies have been done to determine what degree of genetic variation exists between isolates of Puccinia psidii from many different host plants and many different locations (Langrell et al . 2008, Kawanishi et al . 2009, Kadooka 2010, Graça et al . 2011). So far, all of these studies have shown that all of the Hawaiian samples tested so far have had the same genetic composition. Given that the P. psidii strain in Hawai`i has continually been shown for over five years to lack genetic variation at microsatellite marker sites (which are believed to undergo relatively rapid genetic change), a baseline evaluation of incidence and severity should be especially valuable to provide comparisons with future conditions. Worldwide, 23 Neotropical species in 11 genera and 59 Australasian and Pacific species in 13 genera had been recorded as hosts of Puccinia psidii before 2010 (Simpson et al . 2006, Anderson et al . 2007). Of those 82 species known to be hosts elsewhere, 42 are cultivated or naturalized in Hawai`i. Because of its wide host-range and aggressive pathogenicity, rust disease caused by P. psidii poses a considerable disease threat to many native and cultivated Myrtaceae throughout the world (Coutinho et al . 1998, Booth et al . 2000, Simpson et al . 2006). However, there are few reports comparing the severity of rust infection on native, introduced, and cultivated Myrtaceae (Rayachhetry et al . 2001, Perez et al . 2010). Since government agencies and the public are concerned about the extent of the rust movement within and to Hawai`i (Loope and La Rosa 2008, Loope 2010), there is a need to better understand the incidence, severity, and distribution of P. psidii in Hawai`i. To address that need, this research project was initiated to survey forests, surrounding plant communities, botanical gardens, and commercial nurseries to detect the presence and severity of P. psidii rust infections throughout Hawai`i on plants in the Myrtaceae family. This study provides a baseline on the host distribution and severity to compare current and future impacts of rust infections caused by P. psidii on native, naturalized, and cultivated Myrtaceae in Hawai`i.

Hawai'i↗

Coral disease and health workshop: Coral histopathology II, July 12-14, 2005

The health and continued existence of coral reef ecosystems are threatened by an increasing array of environmental and anthropogenic impacts. Coral disease is one of the prominent causes of increased mortality among reefs globally, particularly in the Caribbean. Although over 40 different coral diseases and syndromes have been reported worldwide, only a few etiological agents have been confirmed; most pathogens remain unknown and the dynamics of disease transmission, pathogenicity and mortality are not understood. Causal relationships have been documented for only a few of the coral diseases, while new syndromes continue to emerge. Extensive field observations by coral biologists have provided substantial documentation of a plethora of new pathologies, but our understanding, however, has been limited to descriptions of gross lesions with names reflecting these observations (e.g., black band, white band, dark spot). To determine etiology, we must equip coral diseases scientists with basic biomedical knowledge and specialized training in areas such as histology, cell biology and pathology. Only through combining descriptive science with mechanistic science and employing the synthesis epizootiology provides will we be able to gain insight into causation and become equipped to handle the pending crisis. One of the critical challenges faced by coral disease researchers is to establish a framework to systematically study coral pathologies drawing from the field of diagnostic medicine and pathology and using generally accepted nomenclature. This process began in April 2004, with a workshop titled Coral Disease and Health Workshop: Developing Diagnostic Criteria co-convened by the Coral Disease and Health Consortium (CDHC), a working group organized under the auspices of the U.S. Coral Reef Task Force, and the International Registry for Coral Pathology (IRCP). The workshop was hosted by the U.S. Geological Survey, National Wildlife Health Center (NWHC) in Madison, Wisconsin and was focused on gross morphology and disease signs observed in the field. A resounding recommendation from the histopathologists participating in the workshop was the urgent need to develop diagnostic criteria that are suitable to move from gross observations to morphological diagnoses based on evaluation of microscopic anatomy. As a continuation of building the foundation and framework for coral disease diagnostics, the CDHC convened the Coral Disease and Health Workshop: Coral Histopathology II in Charleston, South Carolina, July 11-14, 2005. The workshop was hosted by the Department of Pathology and Laboratory Medicine at the Medical University of South Carolina, Charleston, SC which provided expertise, facilities and equipment in support of the workshop. All of the histological slides and related photographs used in the discussions were prepared and supplied by the IRCP. This workshop brought together 15 experts in veterinary and medical pathology and coral biology from national and international research institutes and government laboratories. The mission was to devise a standardized approach to examining microscopic anatomy and pathology of corals and a standardized nomenclature to facilitate accurate descriptions of the microscopic morphology of corals and enhance communication among specialists investigating causes of coral death. 2 The participants of this workshop deliberated for 3 days to refine the nomenclature for gross and microscopic anatomy of corals and systematically described microscopic changes associated with selected coral diseases. The findings and recommendations from the deliberations will be submitted to the research community for peer review. The standardized nomenclature and descriptions produced at this workshop will ultimately be made available to the scientific community through a variety of media including the World Wide Web. An exciting highlight of this meeting was provided by Professor Robert Ogilvie (MUSC Department of Cell Biology and Anatomy) when he introduced participants to a new digital technology that is revolutionizing histology and histopathology in the medical field. The Virtual Slide technology creates digital images of histological tissue sections by computer scanning actual slides in high definition and storing the images for retrieval and viewing. Virtual slides now allow any investigator with access to a computer and the web to view, search, annotate and comment on the same tissue sections in real time. Medical and veterinary slide libraries across the country are being converted into virtual slides to enhance biomedical education, research and diagnosis. The coral health and disease researchers at this workshop deem virtual slides as a significant way to increase capabilities in coral histology and a means for pathology consultations on coral disease cases on a global scale.

NOAA Technical Memorandum↗

Controlled field and laboratory studies on VHS and Ichtyophonus in Pacific herring: Section II in Investigations of disease factors affecting declines of Pacific herring populations in Prince William Sound

From 1995 through 1998 the controlled disease studies covered a wide range of topics including virus survival in seawater, development of natural immunity, effects of oil exposure on immunity, effect of synthetic immunosuppressants, epizootiology of VHSV in net pens, antibody production and the natural history of VHS in Pacific herring. Both VHSV and I. hoferi were was observed in fish that reached two-years-old while in captivity. Prior to 2 years old, fish that shown to be. serious pathogens of juvenile hening. A natural age-related resistance to VHS virus plaque assay and resistance to reinfection with the known minimum lethal dose of virus. survived an initial infection by VHSV developed an acquired immunity detectable by in vitro Three years of consecutive monthly sampling of wild 0-year herring in Puget Sound revealed a VHSV carrier rate below 1%, but that this level of virus shedding was adequate to initiate an epizootic under confined conditions, and probably resulted in infection of free-ranging fish also. Over 50% of the virus was recoverable from seawater after 2 hours, was still detectable after six hours, and survived up to 100 h when ovarian fluid was present in the water. Studies in PWS demonstrated that closed pounds play a role in transmission of VHSV to impounded fish steadily increased with confinement time and viral tissue titers were at very high susceptible fish, resulting in the rapid spread of virus within the pens. Prevalence of VHSV from levels in fish being released after 8 days in captivity. Viable virus was also recovered from the water inside and outside the net pens at levels adequate to initiate an epizootic in susceptible fish. of herring and that vitro culture was the most sensitive method for detecting it. Studies on Ichthyophonus hoferi demonstrated that the organism is a potential serious pathogen No evidence for increased susceptibility, mortality or loss of disease resistance was observed in wild or laboratory-reared herring exposed to oil or synthetic corticosteroids, either prior to or following exposure to VHSV.

Report↗

Field performance of cucurbit and tomato plants infected with a nonpathogenic mutant of Colletotrichum magna (teleomorph: Glomerella magna; Jekins and Winstead)

Path-1 is a UV-induced non-pathogenic mutant of a virulent Colletotrichum magna isolate that establishes mutualistic symbioses with cucurbit and tomato species. Under laboratory conditions, this mutualism results in plant growth enhancement, drought tolerance, and disease protection against fungal pathogens. This study focuses on the efficacy of this symbiosis and the symbiotic lifestyle expressed by path-1 under field conditions in the absence of disease stress. The effects of colonization by path-1 on fruit yields and growth was measured in field plots with four cucurbit species including four watermelon cultivars, and two tomato cultivars, over four growing seasons. The persistence of the symbiosis, extent of colonization, and path-1 transmission were also assessed. Yields from path-1 infected plants were equivalent to or greater than yields from non-inoculated control plants and path-1 systemically colonized plants throughout each growing season. Path-1 also increased the growth rates of tomato plants and was not transmitted to uncolonized plants. The results indicate that there are no metabolic costs of this symbiosis and the symbiosis is maintained under field conditions.

Symbiosis↗

Status of whitebarkpine in the Greater Yellowstone Ecosystem: A step-trend analysis comparing 2004-2007 to 2008-2011

Whitebark pine (Pinus albicaulis) is a foundation and keystone species in upper subalpine environments of the northern Rocky Mountains that strongly influences the biodiversity and productivity of high-elevation ecosystems (Tomback et al. 2001, Ellison et al. 2005). Throughout its historic range, whitebark pine has decreased significantly as a major component of high-elevation forests. As a result, it is critical to understand the challenges to whitebark pine—not only at the tree and stand level, but also as these factors influence the distribution of whitebark pine across the Greater Yellowstone Ecosystem (GYE). In 2003, the National Park Service (NPS) Greater Yellowstone Inventory & Monitoring Network identified whitebark pine as one of twelve significant natural resource indicators or vital signs to monitor (Jean et al. 2005, Fancy et al. 2009) and initiated a long-term, collaborative monitoring program. Partners in this effort include the U.S. Geological Survey, U.S. Forest Service, and Montana State University with representatives from each comprising the Greater Yellowstone Whitebark Pine Monitoring Working Group. The objectives of the monitoring program are to assess trends in (1) the proportion of live, whitebark pine trees (>1.4-m tall) infected with white pine blister rust (blister rust); (2) to document blister rust infection severity by the occurrence and location of persisting and new infections; (3) to determine mortality of whitebark pine trees and describe potential factors contributing to the death of trees; and (4) to assess the multiple components of the recruitment of understory whitebark pine into the reproductive population. In this report we summarize the past eight years (2004-2011) of whitebark pine status and trend monitoring in the GYE. Our study area encompasses six national forests (NF), two national parks (NP), as well as state and private lands in portions of Wyoming, Montana, and Idaho; this area is collectively described as the GYE here and in other studies. The sampling design is a probabilistic, twostage cluster design with stands of whitebark pine as the primary units and 10x50 m belt transects as the secondary units. Primary sampling units (stands) were selected randomly from a sample frame of approximately 10,770 mapped pure and mixed whitebark pine stands ≥2.0 hectares in the GYE (Dixon 1997, Landenburger 2012). From 2004 through 2007 (monitoring transect establishment or initial time-step), we established 176 permanent belt transects (secondary sampling units=176) in 150 whitebark pine stands and permanently marked approximately 4,740 individual trees >1.4 m tall to monitor long-term changes in blister rust infection and survival rates. Between 2008 and 2011 (revisit time-step), these same 176 transects were surveyed and again all previously tagged trees were observed for changes in blister rust infection and survival status. Objective 1. Using a combined ratio estimator, we estimated the proportion of live trees infected in the GYE in the initial time-step (2004-2007) to be 0.22 (0.031 SE). Following the completion of all surveys in the revisit time-step (2008-2011), we estimated the proportion of live trees infected with white pine blister rust as 0.23 (0.028 SE; Table 2). We detected no significant change in the proportion of trees infected in the GYE between the two time-steps. Objective 2. We documented blister rust canker locations as occurring in the canopy or bole. We compared changes in canker position between the initial time-step (2004-2007) and the revisit time-step (2008-2011) in order to assess changes in infection severity. This analysis included the 3,795 trees tagged during the initial time-step that were located and documented as alive at the end of the revisit time-step. At the end of the revisit time-step, we found 1,217 trees infected with blister rust. This includes the 287 newly tagged trees in the revisit time step of which 14 had documented infections. Of these 1,217 trees, 780 trees were infected with blister rust in both time steps. Trees with only canopy cankers made up approximately 43% (519 trees) of the total number of trees infected with blister rust at the end of the revisit time-step, while trees with only bole cankers comprised 20% (252 trees), and those with both canopy and bole cankers included 37% (446 trees) of the infected sample. A bole infection is considered to be more consequential than a canopy canker, as it compromises not only the overall longevity of the tree, but its functional capacity for reproductive output as well (Kendall and Arno 1990, Campbell and Antos 2000, McDonald and Hoff 2001, Schwandt and Kegley 2004). In addition to infection location, we also documented infection transition between the canopy and bole. Of the 780 live trees that were infected with blister rust in both time-steps, approximately 31% (242) maintained canopy cankers and 36% (281) retained bole infections at the end of the revisit time-step. Infection transition from canopy to bole occurred in 30% (234) of the revisit time-step trees while 3% (23) transitioned from bole to canopy infections during this period. Objective 3. To determine whitebark pine mortality, we resurveyed all belt transects to reassess the life status of permanently tagged trees >1.4 m tall. We compared the total number of live tagged trees recorded during monitoring transect establishment to the total number of resurveyed dead tagged trees recorded during the revisit time-step and identified all potential mortality-influencing conditions (blister rust, mountain pine beetle, fire and other). By the end of the revisit time-step, we observed a total of 975 dead tagged whitebark pine trees; using a ratio estimator, this represents a loss of approximately 20% (SE=4.35%) of the original live tagged tree population (GYWPMWG 2012). Objective 4. To investigate the proportion of live, reproducing tagged trees, we divided the total number of positively identified cone-bearing trees by the total number of live trees in the tagged tree sample at the end of the revisit time-step. To approximate the average density of recruitment trees per stand, trees ≤1.4 m tall were summed by stand (within the 500 m² transect area) and divided by the total number of stands. Reproducing trees made up approximately 24% (996 trees) of the total live tagged population at the end of the revisit time-step. Differentiating between whitebark pine and limber pine seedlings or saplings is problematic given the absence of cones or cone scars. Therefore, understory summaries as presented in this report may include individuals of both species when they are sympatric in a stand. The average density of small trees ≤1.4 m tall was 53 understory trees per 500 m². Raw counts of these understory individuals ranged from 0-635 small trees per belt transect. In addition, a total of 287 trees were added to the tagged tree population by the end of 2011. These newly tagged trees were individuals that upon subsequent revisits had reached a height of >1.4 m tall and subsequently added to the sample. Throughout the past decade in the GYE, monitoring has helped document shifts in whitebark pine forests; whitebark pine stands have been impacted by insect, pathogen, wildland fire, and other disturbance events. Blister rust infection is ubiquitous throughout the ecosystem and infection proportions are variable across the region. And while we have documented mortality of whitebark pine, we have also recorded considerable recruitment. We provide this first step-trend report as a quantifiable baseline for understanding the state of whitebark pine in the GYE. Many aspects of whitebark pine health are highly variable across the range of its distribution in the GYE. Through sustained implementation of the monitoring program, we will continue efforts to document and quantify whitebark pine forest dynamics as they arise under periodic upsurges in insect, pathogen, fire episodes, and climatic events in the GYE. Since its inception, this monitoring program perseveres as one of the only sustained longterm efforts conducted in the GYE with a singular purpose to track the health and status of this prominent keystone species.

Natural Resource Technical Report↗

NASA and USGS invest in invasive species modeling to evaluate habitat for Africanized Honey Bees

Invasive non-native species, such as plants, animals, and pathogens, have long been an interest to the U.S. Geological Survey (USGS) and NASA. Invasive species cause harm to our economy (around $120 B/year), the environment (e.g., replacing native biodiversity, forest pathogens negatively affecting carbon storage), and human health (e.g., plague, West Nile virus). Five years ago, the USGS and NASA formed a partnership to improve ecological forecasting capabilities for the early detection and containment of the highest priority invasive species. Scientists from NASA Goddard Space Flight Center (GSFC) and the Fort Collins Science Center developed a longterm strategy to integrate remote sensing capabilities, high-performance computing capabilities and new spatial modeling techniques to advance the science of ecological invasions [Schnase et al., 2002].

The Earth Observer↗

Septoria hodgesii sp. nov.: A potential biocontrol agent for Myrica faya in Hawai‘i

Septoria hodgesii sp. nov. is described. This fungus is a common leaf pathogen of Myrica cerifera in the southeastern U.S., where it usually has been identified as S. myricae . It also has been shown by artificial inoculation to be pathogenic on M. faya , an introduced forest weed in Hawai'i. Comparison of S. hodgesii with the types of S. myricae , from M. cerifera and S. myricata , from M. gale , showes it to be distinct from both species.

Hawai'i↗

Effects of climate change on plague exposure pathways and resulting disease dynamics

Introduction and Objectives: Sylvatic plague, a zoonotic flea-borne disease, caused by the bacterium Yersinia pestis , is relevant to the Department of Defense (DOD), because prairie dogs and other susceptible rodents are present on military installations in several western states. Arthropod-borne diseases, like plague, are thought to be particularly sensitive to local climate conditions. Expected changes in temperature and humidity over the next several decades will likely increase the geographical expansion of plague outbreaks in wildlife. Through a combination of field and laboratory work, along with data-driven modeling, we evaluated the potential effects of climate change on plague exposure pathways in prairie dogs and associated rodents to provide guidance to DOD partners regarding the potential for future outbreaks. Briefly, our specific objectives were to determine the relation between local climate conditions and the prevalence of plague and other pathogens while assessing the ecological roles of specific rodent hosts and vector species in plague dynamics, evaluate flea intensity on rodent hosts and in burrows in relation to local climate conditions, and develop models to predict the effects of climate change on plague dynamics. Technical Approach: Using data and samples collected during a large field study on the effectiveness of vaccination to manage plague in prairie dogs, we assessed rodent/flea assemblages, pathogen prevalence in fleas, and determined how local climate conditions influence flea development rates and relative abundance. Live animals (prairie dogs and some small rodents) were trapped to collect fleas and other samples on 46 prairie dog plots in 6 western states, many sites near DOD lands. At seven additional locations on a latitudinal gradient, fleas were collected from burrows several times per year to assess seasonality and effects of local climate conditions on flea abundance. These data were then used to develop predictive models that could be used to test specific hypotheses. Results: We determined that flea developmental rates, on-host flea abundance, species composition of the flea community, and burrow temperatures varied across a latitudinal gradient. Rodent and flea community composition and abundance differed geographically and were highly specialized. Flea-switching between prairie dogs and short-lived rodents was rare. Flea development rates, on-host flea abundance, and burrow temperatures increased with increasing ambient temperature. Although relative humidity can affect flea development, burrow humidity was uniformly high (~85%) across sampling sites and seasons. A large increase in the number of fleas found on a prairie dog colony, coupled with a greater number of infested burrows, could have substantial effects on plague dynamics in the western United States as the climate warms. In addition to affecting flea load, climate change may also influence body condition of prairie dogs by reducing the amount of forage. This may result in animals being more tolerant of high flea loads (less engaged in grooming behavior) and more vulnerable to disease.

Arizona, Montana, South Dakota, Texas, Utah, Wyomi↗

Development and utility of a gene transcription panel for desert bighorn sheep (Ovis canadensis nelsoni)

Respiratory disease is a key factor impacting the success of the ongoing conservation and recovery of wild sheep populations (WAFWA 2017). Although the primary pathogens involved in the bighorn sheep pneumonia complex have been identified, the wide variability in herd response following infection is not well understood (Cassirer et al. 2018). The response of populations infected with Mycoplasma ovipneumoniae has been variable, from minimal to extensive herd mortality followed by years to decades of either poor lamb recruitment or little expression of disease and minimal impact on lamb survival (Coggins and Mathews 1992, Jorgenson et al. 1997, Cassirer et al. 2018). This variation is thought to be caused by differences in pathogen virulence, intrinsic or extrinsic factors that impact individual or herd immunity, including lungworm ( Protostrongylus spp.) or mite ( Psoroptes ovis ) infections, malnutrition, inbreeding, harsh weather conditions, or stress associated with overcrowding (Risenhoover et al. 1988, Bailey 1990, Jones and Worley 1994, Monello et al. 2001). Although substantial management strategies have been implemented, they have been ineffective in halting the spread of the epizootic (Cassirer et al. 2018).

Conference Paper↗

Avian influenza in wild birds

Influenza A viruses (IAVs)maintained among wild waterfowl, gulls, shorebirds, and some seabirds, and typically do not cause disease. Some avian-origin IAVs that have previously spilled over into domestic poultry have developed a highly pathogenic phenotype and have become important pathogens affecting both wild birds and poultry. These avian-origin IAVs have important implications to the production and trade of domestic birds, conservation and management of wild birds, and the risk of spillover of zoonotic influenza to humans handling infected birds.

Book chapter↗

Wildlife health implications of sewage disposal in wetlands

Wildlife health concerns associated with disposal of sewage effluent in wetlands are of three primary types: (1) introduction of pathogens, (2) introduction of pollutants that adversely impact on host body defense mechanisms, and (3) changes in the physical and chemical properties of wetlands that favor the development and maintenance of disease problems. Unlike the situation with human health concerns, introduction of pathogens is not the major concern regarding wildlife health. Instead, the focus of attention needs to be directed at environmental changes likely to take place as a result of effluent discharges into different types of wetlands. Unless these changes are adequately addressed from a disease perspective, marshes utilized for sewage disposal could become disease incubators and wildlife death traps. This result would be unfortunate because the backlash would likely negate the potentially beneficial aspects of the use of sewage wastewater for the creation of new wetlands and have a severe impact on progress being made towards evaluation of the compatibility of wildlife and sewage effluents.

Book chapter↗

Diseases of amphibian eggs and embryos

Amphibians generally are prolific egg producers. In tropical and semi-tropical regions, deposition of eggs may occur year-round or may coincide with rainy seasons, while in temperate regions, deposition of eggs usually occurs immediately after emergence from hibernation. Numbers of eggs produced by each species may vary from a few dozen to thousands. Accordingly, some eggs may be infertile and wastage of embryos is to be expected. Fertility, viability and decomposition of eggs and embryos must be considered before it is assumed that diseases are present. An important consideration in the evaluation of egg masses is the fact that some will contain infertile and non-viable eggs. These infertile and nonviable eggs will undergo decomposition and they may appear similar to eggs that are infected by a pathogen. Evaluation of egg masses and embryos for the presence of disease may require repeated observations in a given breeding season as well as continued monitoring of egg masses during their growth and development and over successive breeding seasons. Amphibian eggs rarely are subjected to a comprehensive health (diagnostic) examination; hence, there is scant literature on the diseases of this life stage. Indeed, the eggs of some North American amphibians have yet to be described. Much basic physiology and normal biomedical baseline data on amphibian eggs is lacking. For example, it is known that the aquatic eggs of some species of shrimp quickly are coated by a protective and commensal bacterium that effectively impedes invasion of the eggs by other environmental organisms and potential pathogens. In the absence of this bacterium, shrimp eggs are rapidly killed by other bacteria and fungi (Green, 2001). The possibility that amphibian eggs also have important symbiotic or commensal bacteria needs to be investigated. Furthermore, the quantity and types of chemicals in the normal gelatinous capsules of amphibian eggs have scarcely been examined. Abnormalities of the female oviduct, either due to infectious disease, nutritional status, hormonal imbalances, or sublethal intoxications, could affect the quality of secreted gelatinous capsules on eggs, thus rendering an egg mass susceptible to other stressors. Diseases of amphibian eggs and embryos presented in this chapter are Lucke frog herpesvirus Ranavirus (iridovirus) infection Bacteria Watermold infection (saprolegniasis) Algae Microsporidia

Book chapter↗

A study of gizzard nematodes and renal coccidiosis in Canada geese (Branta canadensis interior) of the Mississippi Valley population

A total of 309 Mississippi Valley Population Canada geese, Branta canadensis interior , of different sex and age groups was collected from three locations in the Mississippi Flyway from 1979-1981 and examined for gizzard nematodes and renal coccidia. Three species of nematodes were removed from the gizzards, Amidostomum anseris, A. spatulatum, and Epomidiostomum crami. The latter two species are reported from this population of geese for the first time. Gizzard nematodes were found in 95.2% of all Canada geese examined, with A. anseris being the most abundant of the three species. There was no statistically significant difference between immatures and adults in the abundance of total nematodes species however, immature geese carried significantly more A. anseris and adult geese harbored significantly more A. spatulatum and E. crami infections. No significant difference in gizzard worm infections between male and female birds was observed. The abundance of overall gizzard nematodes was greatest in Canada geese from Winisk, Ontario (11.9), but the abundance of worms in southern Illinois geese (10.0) was similar. Geese from Horicon National Wildlife Refuge had the lowest abundance of infection, 7.5. The overall abundance of nematodes showed a general increase the second year of the study in each sex and age group and at each collection area. Each of three species of nematodes was responsible for some degree of damage to the gizzard lining and koilin, but E. crami was the most pathogenic of the species recovered. The occurrence of renal coccidiosis in Canada geese of this flyway is reported for the first time; the etiologic agent is Eimeria clarkei. The oocysts and/or endogenous stages of E. clarkei were present in 6.8% of the Canada geese sampled and this was the only species found. Male and female geese showed no significant differences in E. clarkei infections, however, significantly more immature geese than adult geese were infected with this species. A cell mediated response to the presence of E. clarkei oocysts and endogenous stages was seen in 83.3% of infected adult geese, but only 20% of immature geese showed a macrophage response to the infective stages of this parasite. A massive E. clarkei infection caused the death of one goose collected at Horicon National Wildlife Refuge. Amidostomiasis, epomidiostomiasis, and renal coccidiosis were important pathogenic diseases in the Mississippi Valley Population Canada geese but did not directly cause significant mortality in the population.

Illinois, Ontario, Wisconsin↗

A missing dimension in measures of vaccination impacts

Immunological protection, acquired from either natural infection or vaccination, varies among hosts, reflecting underlying biological variation and affecting population-level protection. Owing to the nature of resistance mechanisms, distributions of susceptibility and protection entangle with pathogen dose in a way that can be decoupled by adequately representing the dose dimension. Any infectious processes must depend in some fashion on dose, and empirical evidence exists for an effect of exposure dose on the probability of transmission to mumps-vaccinated hosts [1] , the case-fatality ratio of measles [2] , and the probability of infection and, given infection, of symptoms in cholera [3] . Extreme distributions of vaccine protection have been termed leaky (partially protects all hosts) and all-or-nothing (totally protects a proportion of hosts) [4] . These distributions can be distinguished in vaccine field trials from the time dependence of infections [5] . Frailty mixing models have also been proposed to estimate the distribution of protection from time to event data [6] , [7] , although the results are not comparable across regions unless there is explicit control for baseline transmission [8] . Distributions of host susceptibility and acquired protection can be estimated from dose-response data generated under controlled experimental conditions [9] – [11] and natural settings [12] , [13] . These distributions can guide research on mechanisms of protection, as well as enable model validity across the entire range of transmission intensities. We argue for a shift to a dose-dimension paradigm in infectious disease science and community health.

PLoS Pathogens↗

Virus shedding kinetics and unconventional virulence tradeoffs

Tradeoff theory, which postulates that virulence provides both transmission costs and benefits for pathogens, has become widely adopted by the scientific community. Although theoretical literature exploring virulence-tradeoffs is vast, empirical studies validating various assumptions still remain sparse. In particular, truncation of transmission duration as a cost of virulence has been difficult to quantify with robust controlled in vivo studies. We sought to fill this knowledge gap by investigating how transmission rate and duration were associated with virulence for infectious hematopoietic necrosis virus (IHNV) in rainbow trout ( Oncorhynchus mykiss ). Using host mortality to quantify virulence and viral shedding to quantify transmission, we found that IHNV did not conform to classical tradeoff theory. More virulent genotypes of the virus were found to have longer transmission durations due to lower recovery rates of infected hosts, but the relationship was not saturating as assumed by tradeoff theory. Furthermore, the impact of host mortality on limiting transmission duration was minimal and greatly outweighed by recovery. Transmission rate differences between high and low virulence genotypes were also small and inconsistent. Ultimately, more virulent genotypes were found to have the overall fitness advantage, and there was no apparent constraint on the evolution of increased virulence for IHNV. However, using a mathematical model parameterized with experimental data, it was found that host culling resurrected the virulence tradeoff and provided low virulence genotypes with the advantage. Human-induced or natural culling, as well as host population fragmentation, may be some of the mechanisms by which virulence diversity is maintained in nature. This work highlights the importance of considering non-classical virulence tradeoffs.

PLoS Pathogens↗

Infectivity of wild-bird origin Influenza A viruses in Minnesota wetlands across seasons

The environmental tenacity of influenza A viruses (IAVs) in the environment likely plays a role in their transmission; IAVs are able to remain infectious in aquatic habitats and may have the capacity to seed outbreaks when susceptible wild bird hosts utilize these same environments months or even seasons later. Here, we aimed to assess the persistence of low-pathogenicity IAVs from naturally infected ducks in Northwestern Minnesota through a field experiment. Viral infectivity was measured using replicate samples maintained in distilled water in a laboratory setting as well as in filtered water from four natural water bodies maintained in steel perforated drums (hereafter, mesocosms) within the field from autumn 2020 to spring 2021. There was limited evidence for the extended persistence of IAVs held in mesocosms; from 65 initial IAV-positive samples, only six IAVs persisted to at least 202 days in the mesocosms compared to 17 viruses persisting at least this long when held under temperature-controlled laboratory settings in distilled water. When accounting for the initial titer of samples, viruses detected at a higher concentration at the initiation of the experiment persisted longer than those with a lower starting titer. A parallel experimental laboratory model was used to further explore the effects of water type on viral persistence, and the results supported the finding of reduced tenacity of IAVs held in mesocosms compared to distilled water. The results of this investigation provide evidence that many factors, including temperature and physicochemical properties, impact the duration of viral infectivity in natural settings, further extending our understanding of the potential and limitations of environmental-based methodologies to recover infectious IAVs.

Minnesota↗