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At least 73 records · Page 4Linked to original sources
USGS2014

Tick control: Trapping, bio-control, host management and other alternative strategies

Biology of Ticks is the most comprehensive work on tick biology and tick-borne diseases. This second edition is a multi-authored work, featuring the research and analyses of renowned experts across the globe. Spanning two volumes, the book examines the systematics, biology, structure, ecological adaptations, evolution, genomics and the molecular processes that underpin the growth, development and survival of these important disease-transmitting parasites. Also discussed is the remarkable array of diseases transmitted (or caused) by ticks, as well as modern methods for their control. This book should serve as a modern reference for students, scientists, physicians, veterinarians and other specialists. Volume II includes chapters on the ecology of non-nidicolous and nidicolous ticks, genetics and genomics (including the genome of the Lyme disease vector Ixodes scapularis) and immunity, including host immune responses to tick feeding and tick-host interactions, as well as the tick's innate immune system that prevents and/or controls microbial infections. Six chapters cover in depth the many diseases caused by the major tick-borne pathogens, including tick-borne protozoa, viruses, rickettsiae of all types, other types of bacteria (e.g., the Lyme disease agent) and diseases related to tick paralytic agents and toxins. The remaining chapters are devoted to tick control using vaccines, acaricides, repellents, biocontrol, and, finally, techniques for breeding ticks in order to develop tick colonies for scientific study.

Book chapter↗
USGS2026

Biomarkers of mortality risks in Yukon Chinook salmon

Premature mortality of spawning adult Pacific salmon ( Oncorhynchus species) can strongly influence population dynamics and complicate escapement-based management. Heat stress and Ichthyophonus infections have been identified as probable drivers of premature mortality in Yukon River Chinook salmon ( Oncorhynchus tshawytscha ) and likely contributors to low spawning abundance. We leveraged a multiagency study focused on Ichthyophonus using lethally collected heart tissue as a rare opportunity to investigate these two stressors jointly in the same individuals to accomplish two tasks: (1) provide a more comprehensive premature mortality risk index that combines heat stress and Ichthyophonus detection and (2) investigate the feasibility of using skeletal muscle tissue gene transcription (mRNA of select genes) as a non-lethal biomarker of Ichthyophonus . Water temperatures ranged from ~12–22°C across four sites and two years. In both 2023 and 2024, effects were identified in ~30% of salmon at Pilot Station, Alaska, and ~70% of salmon by the time they reached mid river (Rapids, Fort Yukon). Mortality risk is presumably highest among fish with multiple stressors, which were detected in ~25% of Chinook salmon in the middle river sites in 2023 when it was warmer and 9—18% in 2024 when it was cooler. We explored Chinook salmon genes that respond to Ichthyophonus with a full transcriptome analysis that measured mRNA of 17,569 genes and identified 53 that were related to Ichthyophonus infection. The differentially expressed genes and their pathways included those known for involvement in immune functions, energy synthesis, cellular breakdown, and reproduction– all processes known to be influenced by senescence during spawning migrations and imply accelerated senescence of infected fish. Primers were developed for 21 of the differentially expressed Chinook salmon genes for qPCR measurements of their mRNA that could be used in classification models. Attempts to statistically deduce Ichthyophonus infection from Chinook salmon gene transcription at the individual and group levels included some potential for separating fish where Ichthyophonus was not detected compared to those with high infection intensities (as judged by qPCR that directly detects Ichthyophonus DNA). Fish with relatively low infection intensities did not have a separate gene transcription signature and grouped with the undetected Ichthyophonus fish in two-thirds of the cases and high infection in onethird of cases. Among the genes with the most utility to predict Ichthyophonus infection were retinoic acid receptor beta (regulates cellular states) and lysozyme CII (immune system gene). Interannual variation in the gene transcription of fish with undetected Ichthyophonus was a complicating factor that demonstrated a need for additional refinement and testing. Overall, this study identified two broad findings: (1) The proportion of migrating fish with one or both of the assessed stressors ( Ichthyophonus infections and/or elevated levels of heat shock protein) can be very high (~70%) and (2) we recommend measuring interannual variation of gene transcription in any study that seeks to develop gene transcription as a biomarker.

Alaska↗
USGS2011

Experimental infection of bats with Geomyces destructans causes white-nose syndrome

White-nose syndrome (WNS) has caused recent catastrophic declines among multiple species of bats in eastern North America. The disease's name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin (including the muzzle) of hibernating bats. Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS. However, the role of G. destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking. The debate is fuelled, in part, by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction. Additionally, the recent discovery that G. destructans commonly colonizes the skin of bats of Europe, where no unusual bat mortality events have been reported, has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS. Here we demonstrate that exposure of healthy little brown bats (Myotis lucifugus) to pure cultures of G. destructans causes WNS. Live G. destructans was subsequently cultured from diseased bats, successfully fulfilling established criteria for the determination of G. destructans as a primary pathogen. We also confirmed that WNS can be transmitted from infected bats to healthy bats through direct contact. Our results provide the first direct evidence that G. destructans is the causal agent of WNS and that the recent emergence of WNS in North America may represent translocation of the fungus to a region with a naive population of animals. Demonstration of causality is an instrumental step in elucidating the pathogenesis and epidemiology of WNS and in guiding management actions to preserve bat populations against the novel threat posed by this devastating infectious disease. ?? 2011 Macmillan Publishers Limited. All rights reserved.

Nature↗
USGS2022

A novel approach for directly incorporating disease into fish stock assessment: A case study with seroprevalence data

When estimating mortality from disease with fish population models, common disease surveillance data such as infection prevalence are not always informative, especially for fast-acting diseases that may go unobserved in infrequently sampled populations. In these cases, seroprevalence — the proportion of fish with measurable antibody levels in their blood — may be more informative. In cases of life-long immunity, seroprevalence data require less frequent sampling intervals than infection prevalence data and can reflect the cumulative exposure history of fish. We simulation tested the usefulness of seroprevalence data in an age-structured fish stock assessment model using viral hemorrhagic septicemia virus (VHSV) in Pacific herring ( Clupea pallasii ) as a case study. We developed a novel epidemiological model to simulate population dynamics and seroprevalence data and fitted to these data in an integrated catch-at-age model with equations that estimate age- and time-varying mortality from disease. We found that simulated seroprevalence data can provide accurate estimates of infection history and disease-associated mortality. Importantly, even models that misspecified nonstationary processes in background or disease-associated mortality, but included seroprevalence data, accurately estimated annual infection and population abundance.

Canadian Journal of Fisheries and Aquatic Sciences↗
USGS2013

Cutthroat trout virus as a surrogate in vitro infection model for testing inhibitors of hepatitis E virus replication

Hepatitis E virus (HEV) is one of the most important causes of acute hepatitis worldwide. Although most infections are self-limiting, mortality is particularly high in pregnant women. Chronic infections can occur in transplant and other immune-compromised patients. Successful treatment of chronic hepatitis E has been reported with ribavirin and pegylated interferon-alpha, however severe side effects were observed. We employed the cutthroat trout virus (CTV), a non-pathogenic fish virus with remarkable similarities to HEV, as a potential surrogate for HEV and established an antiviral assay against this virus using the Chinook salmon embryo (CHSE-214) cell line. Ribavirin and the respective trout interferon were found to efficiently inhibit CTV replication. Other known broad-spectrum inhibitors of RNA virus replication such as the nucleoside analog 2′-C-methylcytidine resulted only in a moderate antiviral activity. In its natural fish host, CTV levels largely fluctuate during the reproductive cycle with the virus detected mainly during spawning. We wondered whether this aspect of CTV infection may serve as a surrogate model for the peculiar pathogenesis of HEV in pregnant women. To that end the effect of three sex steroids on in vitro CTV replication was evaluated. Whereas progesterone resulted in marked inhibition of virus replication, testosterone and 17β-estradiol stimulated viral growth. Our data thus indicate that CTV may serve as a surrogate model for HEV, both for antiviral experiments and studies on the replication biology of the Hepeviridae.

Antiviral Research↗
USGS2026

Stochastic within-host dynamics and climate-sensitive traits generate predictable patterns of variation in disease outcomes

Understanding how climatic variables impact host-pathogen relationships in temperature-sensitive ectothermic host organisms is crucial under global change. Few studies have explored how temperature gradients generate inter-individual variation in epidemiological traits like host susceptibility or pathogen replication. Here, we develop a mathematical model to explore a novel hypothesis: stochastic within-host dynamics and simulated thermal mismatches between host and pathogen traits generate predictable variation in infection outcomes among hosts and across thermal gradients. Our model demonstrates that varying trait thermal optima in host immunity and pathogen replication, and stochastic within-host processes produced variation in infection outcomes. Variability was low when temperatures strongly favored host or pathogen traits, but high and diverse when their performance was similar across a broad thermal range. In contrast, when trait performance was equal across all temperatures (no mismatch) variability remained low at all temperatures. Further, the magnitude of variation, quantified by entropy, exhibited predictable patterns depending on host-pathogen thermal mismatches. We conclude that interactions between trait thermal mismatches and within-host stochasticity provide a theoretical framework to improve ectotherm disease models under climate change, providing a valuable tool for exploring the impacts of environmental change on epizootic or epidemic dynamics, particularly in vulnerable marine ecosystems.

Philosophical Transactions of the Royal Society, S↗
USGS2010

Transcriptome analysis of rainbow trout infected with high and low virulence strains of Infectious hematopoietic necrosis virus

There are three main genetic lineages or genogroups of Infectious hematopoietic necrosis virus (IHNV) in N. America. Strains representing the M genogroup are more virulent in rainbow trout relative to the U genogroup. In this study, we used microarray analysis to evaluate potential mechanisms responsible for host-specific virulence in rainbow trout that were given intraperitoneal injections of buffer or a representative M or U type virus strain. Reverse transcriptase quantitative PCR (RT-qPCR) was used to assess viral load and gene expression of select immune genes. Viral load was significantly higher in trout infected with the M virus starting at 24 h post-infection (p.i.) and continuing until 72 h p.i. Microarray analysis of the 48 h time point revealed 153 up-regulated and 248 down-regulated features in response to M virus infection but only 62 up-regulated and 49 down-regulated features following U virus infection. Translation and transcription features were among the most frequent down-regulated features in response to M virus infection and may be associated with the host cell shutoff phenomenon. A greater host cell shutoff response by the M virus may facilitate subversion of the host cell transcriptional machinery and enhance viral replication, suggesting the M virus may be better optimized to manipulate the rainbow trout transcriptional and translational machinery. Anti-viral associated features were the most commonly up-regulated features. A common set of features were up-regulated in both the M and U infection groups, but were induced to a higher magnitude in the M infection group. Gene expression of the anti-viral genes Mx-1 and Vig-1 was correlated but not entirely dependent on viral load in the anterior kidney. Slower replication of the U virus may allow the host more time to induce protective anti-viral immune mechanisms.

Fish and Shellfish Immunology↗
USGS2011

Influence of body condition on influenza A virus infection in mallard ducks: Experimental infection data

Migrating waterfowl are implicated in the global spread of influenza A viruses (IAVs), and mallards ( Anas platyrhynchos ) are considered a particularly important IAV reservoir. Prevalence of IAV infection in waterfowl peaks during autumn pre-migration staging and then declines as birds reach wintering areas. Migration is energetically costly and birds often experience declines in body condition that may suppress immune function. We assessed how body condition affects susceptibility to infection, viral shedding and antibody production in wild-caught and captive-bred juvenile mallards challenged with low pathogenic avian influenza virus (LPAIV) H5N9. Wild mallards (n = 30) were separated into three experimental groups; each manipulated through food availability to a different condition level (-20%, -10%, and normal ±5% original body condition), and captive-bred mallards (n = 10) were maintained at normal condition. We found that wild mallards in normal condition were more susceptible to LPAIV infection, shed higher peak viral loads and shed viral RNA more frequently compared to birds in poor condition. Antibody production did not differ according to condition. We found that wild mallards did not differ from captive-bred mallards in viral intensity and duration of infection, but they did exhibit lower antibody titers and greater variation in viral load. Our findings suggest that reduced body condition negatively influences waterfowl host competence to LPAIV infection. This observation is contradictory to the recently proposed condition-dependent hypothesis, according to which birds in reduced condition would be more susceptible to IAV infection. The mechanisms responsible for reducing host competency among birds in poor condition remain unknown. Our research indicates body condition may influence the maintenance and spread of LPAIV by migrating waterfowl.

Michigan↗
USGS2018

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↗
USGS2009

Oral and parenteral immunization of chickens (Gallus gallus) against West Nile virus with recombinant envelope protein

West Nile virus (WNV) causes morbidity and mortality in humans, horses, and in more than 315 bird species in North America. Currently approved WNV vaccines are designed for parenteral administration and, as yet, no effective oral WNV vaccines have been developed. WNV envelope (E) protein is a highly antigenic protein that elicits the majority of virus-neutralizing antibodies during a WNV immune response. Leghorn chickens were given three vaccinations (each 2 wk apart) of E protein orally (20 ??g or 100 ??g/dose), of E protein intramuscularly (IM, 20 ??g/dose), or of adjuvant only (control group) followed by a WNV challenge. Viremias were measured post-WNV infection, and three new enzyme-linked immunosorbent assays were developed for quantifying IgM, IgY, and IgA-mediated immune response of birds following WNV infection. WNV viremia levels were significantly lower in the IM group than in both oral groups and the control group. Total WNV E protein-specific IgY production was significantly greater, and WNV nonstructural 1-specific IgY was significantly less, in the IM group compared to all other treatment groups. The results of this study indicate that IM vaccination of chickens with E protein is protective against WNV infection and results in a significantly different antibody production profile as compared to both orally vaccinated and nonvaccinated birds. ?? 2009 American Association of Avian Pathologists.

Wisconsin↗
USGS2013

Experimental infection studies demonstrating Atlantic salmon as a host and reservoir of viral hemorrhagic septicemia virus type IVa with insights into pathology and host immunity

In British Columbia, Canada (BC), aquaculture of finfish in ocean netpens has the potential for pathogen transmission between wild and farmed species due to the sharing of an aquatic environment. Viral hemorrhagic septicemia virus (VHSV) is enzootic in BC and causes serious disease in wild Pacific herring, Clupea pallasii, which often enter and remain in Atlantic salmon, Salmo salar, netpens. Isolation of VHSV from farmed Atlantic salmon has been previously documented, but the effects on the health of farmed salmon and the wild fish sharing the environment are unknown. To determine their susceptibility, Atlantic salmon were exposed to a pool of 9 isolates of VHSV obtained from farmed Atlantic salmon in BC by IP-injection or by waterborne exposure and cohabitation with diseased Pacific herring. Disease intensity was quantified by recording mortality, clinical signs, histopathological changes, cellular sites of viral replication, expression of interferon-related genes, and viral tissue titers. Disease ensued in Atlantic salmon after both VHSV exposure methods. Fish demonstrated gross disease signs including darkening of the dorsal skin, bilateral exophthalmia, light cutaneous hemorrhage, and lethargy. The virus replicated within endothelial cells causing endothelial cell necrosis and extensive hemorrhage in anterior kidney. Infected fish demonstrated a type I interferon response as seen by up-regulation of genes for IFNα, Mx, and ISG15. In a separate trial infected salmon transmitted the virus to sympatric Pacific herring. The results demonstrate that farmed Atlantic salmon can develop clinical VHS and virus can persist in the tissues for at least 10 weeks. Avoiding VHS epizootics in Atlantic salmon farms would limit the potential of VHS in farmed Atlantic salmon, the possibility for further host adaptation in this species, and virus spillback to sympatric wild fishes.

Veterinary Microbiology↗
USGS2022

Using transcriptomics to predict and visualize disease status in bighorn sheep (Ovis canadensis)

Increasing risk of pathogen spillover coupled with overall declines in wildlife population abundance in the Anthropocene make infectious disease a relevant concern for species conservation worldwide. While emerging molecular tools could improve our diagnostic capabilities and give insight into mechanisms underlying wildlife disease risk, they have rarely been applied in practice. Here, employing a previously reported gene transcription panel of common immune markers to track physiological changes, we present a detailed analysis over the course of both acute and chronic infection in one wildlife species where disease plays a critical role in conservation, bighorn sheep ( Ovis canadensis ). Differential gene transcription patterns distinguished between infection statuses over the course of acute infection and differential correlation (DC) analyses identified clear changes in gene co-transcription patterns over the early stages of infection, with transcription of four genes—TGFb, AHR, IL1b and MX1—continuing to increase even as transcription of other immune-associated genes waned. In a separate analysis, we considered the capacity of the same gene transcription panel to aid in differentiating between chronically infected animals and animals in other disease states outside of acute disease events (an immediate priority for wildlife management in this system). We found that this transcription panel was capable of accurately identifying chronically infected animals in the test dataset, though additional data will be required to determine how far this ability extends. Taken together, our results showcase the successful proof of concept and breadth of potential utilities that gene transcription might provide to wildlife disease management, from direct insight into mechanisms associated with differential disease response to improved diagnostic capacity in the field.

Conservation Physiology↗
USGS2005

Xenobiotics: Chapter 15

While a number of compounds have been reported as toxic to amphibians, until recently, there have been conspicuously few ecotoxicological studies concerning amphibians. Studies are now focusing on the effects of xenobiotics on amphibians, an interest likely stimulated by widespread reports of amphibian declines. It has been speculated that chemical contamination may be partially to blame for some documented amphibian declines, by disrupting growth, reproduction, and behavior. However, evidence that xenobiotics are directly to blame for population declines is sparse because environmental concentrations are typically not great enough to generate direct mortality. Although the effects of environmental contaminants on the amphibian immune system are currently unknown, it is possible that exposure to stressors such as organic pollutants (which enter ecosystems in the form of pesticides) may depress immune system function, thus allowing greater susceptibility to fungal infections. This chapter discusses toxicity testing for xenobiotics and presents the results of a study that has focused on the subtle effects of sublethal concentrations of the chemical carbaryl on tadpoles.

Book chapter↗
USGS2025

Perfluorodecanoic acid (PFDA) disrupts immune regulation via the toll-like receptor signaling pathway in zebrafish

As there are a growing number of per- and polyfluoroalkyl substances (PFAS) alternative substitutes applied globally, it remains paramount to characterize their potential health risks. Perfluorodecanoic acid (PFDA) is the most common alternative PFAS detected in the environment; however, its toxic effects and underlying mechanism of action to aquatic biota remains unclear. In this study, we present in vitro evidence of PFDA-induced immunotoxicity and gain insight into underlying molecular mechanisms. PFDA induced immune dysfunction in zebrafish primarily through immunosuppression, apoptosis, and inflammatory response which further cascaded to suppress innate and adaptive immunities, ultimately weaking the ability of larvae to defend against pathogenic infection. PFDA-induced immunotoxicity was driven by a dysregulation in the toll-like receptor (TLR) signaling pathway, which was validated through a cotreatment of PFDA with either a morpholino knockdown or inhibitor of myeloid differentiation factor 88. Comparative toxicity studies were carried out with a subset of other alternative PFAS (PFBA, PFOA, PFNA) and it was found that PFDA posed a greater immunotoxic response than other commonly identified PFAS in the environment. This work identified a major target of PFDA, disrupting immune function through the TLR signaling pathway, while inducing a greater toxic response among other tested PFAS, which provides novel insights into understanding the potential environmental risks of PFAS substitutes.

Environmental Science & Technology↗
USGS2017

Virulence of a chimeric recombinant infectious haematopoietic necrosis virus expressing the spring viraemia of carp virus glycoprotein in salmonid and cyprinid fish

Infectious haematopoietic necrosis virus (IHNV) and spring viraemia of carp virus (SVCV) are both rhabdoviruses of fish, listed as notifiable disease agents by the World Organization for Animal Health. Recombinant rhabdoviruses with heterologous gene substitutions have been engineered to study genetic determinants and assess the potential of these recombinant viruses for vaccine development. A recombinant IHNV (rIHNV), containing the full-length genome of a European IHNV strain, was modified by deleting the glycoprotein (G) gene and replacing it with a European SVCV G-gene to make the rIHNV-Gsvcv. The chimeric rIHNV-Gsvcv level of virulence in rainbow trout, common carp and koi was assessed, and its ability to induce a protective immune response in surviving koi against wild-type SVCV infection was tested. The rIHNV-Gsvcv infection of trout led to high mortality, ranging from 78% to 92.5%, after immersion. In contrast, no deaths occurred in juvenile common carp after infection with rIHNV-Gsvcv by either immersion or intraperitoneal (IP) injection. Similarly, koi infected with rIHNV-Gsvcv via IP injection had little to no mortality (≤9%). Koi that survived initial infection with a high dose of recombinant virus rIHNV-Gsvcv were protected against a virulent SVCV challenge resulting in a high relative per cent survival of 82.5%.

Journal of Fish Diseases↗
USGS2013

Prevalence of neutralizing antibodies to rabies virus in serum of seven species of insectivorous bats from Colorado and New Mexico, United States

We determined the presence of rabies-virus-neutralizing antibodies (RVNA) in serum of 721 insectivorous bats of seven species captured, sampled, and released in Colorado and New Mexico, United States in 2003-2005. A subsample of 160 bats was tested for rabies-virus RNA in saliva. We sampled little brown bats (Myotis lucifugus) at two maternity roosts in Larimer County, Colorado; big brown bats (Eptesicus fuscus) at three maternity roosts in Morgan County, Colorado; and big brown bats at five maternity roosts in Larimer County. We also sampled hoary bats (Lasiurus cinereus) and silver-haired bats (Lasionycteris noctivagans) captured while drinking or foraging over water in Bernalillo County, New Mexico and at various locations in Larimer County. Big brown bats, little brown bats, long-legged myotis (Myotis volans), long-eared myotis (Myotis evotis), and fringed myotis (Myotis thysanodes) were also sampled over water in Larimer County. All species except long-eared myotis included individuals with RVNA, with prevalences ranging from 7% in adult female silver-haired bats to 32% in adult female hoary bats. None of the bats had detectable rabies-virus RNA in oropharyngeal swabs, including 51 bats of 5 species that had RVNA in serum. Antibody-positive bats were present in nine of the 10 maternity colonies sampled. These data suggest that wild bats are commonly exposed to rabies virus and develop a humoral immune response suggesting some degree of viral replication, but many infections fail to progress to clinical disease.

Colorado;New Mexico↗
USGS2013

Immunological markers for tolerance to avian malaria in Hawai`i `Amakihi: new tools for restoring native Hawaiian forest birds?

We evaluated three assays for non-specific or innate immune capacity to see if measurements were independent of malarial infection and capable of distinguishing malaria-tolerant, low-elevation Hawaiʽi ʽAmakihi from malaria-susceptible, high-elevation ʽAmakihi. ʽAmakihi were captured at Malama Ki Forest Reserve (20 m), Hakalau Forest National Wildlife Refuge (1800 m), and Upper Waiakea Forest Reserve (1700 m), bled for collection of plasma and packed erythrocytes for malarial diagnostics, and either transported to Kīlauea Field Station Aviary and held in captivity for 48 hours for inoculation of wing webs with phytohemagglutinin A (PHA) or released immediately in the field after collection of a blood sample. All birds were tested by polymerase chain reaction (PCR) and microscopy to determine infection status. We found no significant association between malarial infection status and degree of wing web swelling after inoculation with PHA (T = -0.174, df = 13, P = 0.864) and no association between origin of birds from low- and high-elevation populations and degree of wing web swelling (T = 0.113, df = 52, P = 0.911). Infected ʽAmakihi from low elevation had significantly higher small molecule plasma antioxidant capacity than uninfected individuals from the same population (T = -2.675, df = 21, P = 0.014), so we limited comparisons to uninfected birds. Uninfected ʽAmakihi from low elevations did not differ in small molecule plasma antioxidant capacity from uninfected ʽAmakihi from high elevation (T = -0.260, df = 46, P = 0.796). Compared to high-elevation birds, low-elevation ʽAmakihi had significantly higher titers of natural antibodies (NAb) as measured by complement-mediated lysis of rabbit erythrocytes (Mann-Whitney U = 27, X 2 = 32.332, df = 1, P < 0.0001). This innate immunological difference may be related to ability to survive malarial infection and may prove to be important for understanding possible mechanisms for the evolution of disease tolerance in Hawaiʽi’s native bird species.

Hawai'i↗
USGS1999

Duck plague

Duck plague is caused by a herpesvirus. Infection often results in an acute, contagious, and fatal disease. As with many other herpesviruses, duck plague virus can establish inapparent infections in birds that survive exposure to it, a state referred to as latency. During latency, the virus cannot be detected by standard methods for virus isolation. Studies of domestic species of waterfowl have detected multiple strains of the virus that vary in their ability to cause disease and death. Little is known about the response of wild waterfowl to strain differences. Duck plague outbreaks are thought to be caused when birds that carry the virus shed it through fecal or oral discharge, thus releasing the virus into food and water with which susceptible birds may have contact. Experimental studies have demonstrated spontaneous virus shedding by duck plague carriers during spring. Changes in the duration of daylight and onset of breeding are thought to be physiological stresses that stimulate virus shedding at this time of year. The carriers are immune to the disease, but the virus shed by them causes infection and disease among susceptible waterfowl. Bird-to-bird contact and contact with virus that has contaminated the environment perpetuate an outbreak. Scavenging and decomposition of carcasses of infected birds also contaminate the environment by releasing viruses from tissues and body fluids. Virus transmission through the egg has been reported, but the role of the egg in the disease cycle remains to be resolved.

Information and Technology Report↗