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Animal Diseases - Top 30 Publications

Visceral leishmaniasis in an environmentally protected area in southeastern Brazil: Epidemiological and laboratory cross-sectional investigation of phlebotomine fauna, wild hosts and canine cases.

Leishmaniasis is a rapidly expanding zoonosis that shows increasing urbanization. Concern exists regarding the role of wildlife in visceral leishmaniasis (VL) transmission, due to frequent natural or anthropogenic environmental changes that facilitate contact between wildlife, humans and their pets. The municipality of Campinas, in southeastern Brazil, initially recorded VL in 2009, when the first autochthonous case was confirmed in a dog living in an upscale residential condominium, located inside an environmentally protected area (EPA). Since then, disease transmission remains restricted to dogs inhabiting two geographically contiguous condominiums within the EPA.

A novel VWF variant associated with type 2 von Willebrand disease in German Wirehaired Pointers and German Shorthaired Pointers.

Von Willebrand disease (VWD), caused by deficiency of the von Willebrand factor (VWF), is the most common bleeding disorder in humans and dogs. The complete cDNA encoding VWF of a German Wirehaired Pointer with type 2 VWD was sequenced, and we found four variants that alter the amino acid sequence. These variants were: c.1657T>G corresponding to p.Trp553Gly; c.1777G>A (p.Glu593Lys); c.4937A>G (p.Asn1646Ser) and c.5544G>A (p.Met1848Ile). A haplotype of the c.1657G, c.1777A and c.4937G alleles co-segregated with the VWF antigen level in a four-generation pedigree with the disease. Healthy dogs of the breed were found that were homozygous for the c.1777A or the c.5544A allele, indicating that these variants do not cause VWD. Dogs that were homozygous for the c.4937G allele and had no signs of a bleeding disorder were observed in the Chinese Crested dog breed. Thus, only the c.1657G variant was found in the homozygous state exclusively in VWD affecteds, and this variant is the strongest candidate to be the cause of VWD type 2 in the German Wirehaired Pointer breed. A screen of German Shorthaired Pointers indicated that the variant also segregates with VWD in this breed.

Babesiosis Surveillance - Wisconsin, 2001-2015.

Babesiosis is an emerging zoonotic disease caused primarily by Babesia microti, an intraerythocytic protozoan. Babesia microti, like the causal agents for Lyme disease and anaplasmosis, is endemic to the northeastern and upper midwestern United States where it is usually transmitted by the blacklegged tick, Ixodes scapularis. Although babesiosis is usually a mild to moderate illness, older or immunocompromised persons can develop a serious malaria-like illness that can be fatal without prompt treatment. The most common initial clinical signs and symptoms of babesiosis (fever, fatigue, chills, and diaphoresis) are nonspecific and present diagnostic challenges that can contribute to delays in diagnosis and effective treatment with atovaquone and azithromycin (1). Results of one study revealed a mean delay of 12-14 days from symptom onset to treatment (2). Knowledge of the incidence and geographic distribution of babesiosis can raise the index of clinical suspicion and facilitate more prompt diagnosis and lifesaving treatment (1). The first known case of babesiosis in Wisconsin was detected in 1985 (3), and babesiosis became officially reportable in the state in 2001. Wisconsin babesiosis surveillance data for 2001-2015 were analyzed in 3-year intervals to compare demographic, epidemiologic, and laboratory features among patients with cases of reported babesiosis. To determine possible reasons for an increase in reported Babesia infection, trends in electronic laboratory reporting and diagnosis by polymerase chain reaction testing (PCR) were examined. Between the first and last 3-year analysis intervals, there was a 26-fold increase in the incidence of confirmed babesiosis, in addition to geographic expansion. These trends might be generalizable to other states with endemic disease, similar suburbanization and forest fragmentation patterns, and warming average temperatures (4). Accurate surveillance in states where babesiosis is endemic is necessary to estimate the increasing burden of babesiosis and other tickborne diseases and to develop appropriate public health interventions for prevention and practice.

Evolution of Bovine viral diarrhea virus in Canada from 1997 to 2013.

Bovine viral diarrhea virus (BVDV) is a rapidly evolving, single-stranded RNA virus and a production limiting pathogen of cattle worldwide. 79 viral isolates collected between 1997 and 2013 in Canada were subjected to next-generation sequencing. Bayesian phylogenetics was used to assess the evolution of this virus. A mean substitution rate of 1.4×10(-3) substitutions/site/year was found across both BVDV1 and BVDV2. Evolutionary rates in the E2 gene were slightly faster than other regions. We also identified population structures below the sub-genotype level that likely have phenotypic implications. Two distinct clusters within BVDV2a are present and can be differentiated, in part, by a tyrosine to isoleucine mutation at position 963 in the E2 protein, a position implicated in the antigenicity of BVDV1 isolates. Distinct clustering within all sub-genotypes, particularly BVDV2a, is apparent and could lead to new levels of genotypic classification. Continuous monitoring of emerging variants is therefore necessary.

Recognising clinical avian botulism in wild waterbirds.

This article has been prepared by Paul Duff and colleagues of the APHA Wildlife Expert Group.

Disease surveillance in England and Wales, June 2017.

Current and emerging issues: update on Schmallenberg virusHighlights from the scanning surveillance networkUpdate on international disease threatsFocus on recognising clinical avian botulism in wild waterbirdsThese are among matters discussed in the Animal and Plant Health Agency's (APHA's) disease surveillance report for June 2017.

Intrinsic and extrinsic factors related to pathogen infection in wild small mammals in intensive milk cattle and swine production systems.

Understanding the ecological processes that are involved in the transmission of zoonotic pathogens by small mammals may aid adequate and effective management measures. Few attempts have been made to analyze the ecological aspects that influence pathogen infection in small mammals in livestock production systems. We describe the infection of small mammals with Leptospira spp., Brucella spp., Trichinella spp. and Cysticercus fasciolaris and assess the related intrinsic and extrinsic factors in livestock production systems in central Argentina at the small mammal community, population and individual levels.

Invasive forms of canine endoparasites as a potential threat to public health - A review and own studies.

[b]Abstract [/b] Dogs serve as the vectors of serious zoonotic parasitic diseases. In the month of May 2012 - 2014, 339 dog faeces samples from seven public sites in Chełmno, a town in northern Poland, were collected and examined to determine the gastrointestinal parasite fauna of dogs. Each faecal sample was dissected with a needle, checked for tapeworm segments and examined for parasite eggs and oocysts using the flotation and decantation method and a modified Baermann technique. Differences were observed in the degree of parasite species occurrence. The most dominant were [i]Toxocara canis[/i] and Ancylostomatidae. The detected species included: [i]T. canis [/i]and [i]Toxascaris leonina[/i] eggs (23.4% and 10.2%, respectively), as well as eggs from the[i] Ancylostomatidae[/i] family (16.2%),[i] Trichuris vulpis [/i]eggs (6.6%), [i]Taenia[/i] type eggs (4.6%),[i] Dipylidium caninum[/i] (5.2%) and [i]Cystoisospora [/i](Isospora) spp. oocysts (10.9%).

Leptospira diversity in animals and humans in Tahiti, French Polynesia.

Leptospirosis is a highly endemic bacterial zoonosis in French Polynesia (FP). Nevertheless, data on the epidemiology of leptospirosis in FP are scarce. We conducted molecular studies on Leptospira isolated from humans and the potential main animal reservoirs in order to identify the most likely sources for human infection.

Differential replication of Foot-and-mouth disease viruses in mice determine lethality.

Adult C57BL/6J mice have been used to study Foot-and-mouth disease virus (FMDV) biology. In this work, two variants of an FMDV A/Arg/01 strain exhibiting differential pathogenicity in adult mice were identified and characterized: a non-lethal virus (A01NL) caused mild signs of disease, whereas a lethal virus (A01L) caused death within 24-48h independently of the dose used. Both viruses caused a systemic infection with pathological changes in the exocrine pancreas. Virus A01L reached higher viral loads in plasma and organs of inoculated mice as well as increased replication in an ovine kidney cell line. Complete consensus sequences revealed 6 non-synonymous changes between A01L and A10NL genomes that might be linked to replication differences, as suggested by in silico prediction studies. Our results highlight the biological significance of discrete genomic variations and reinforce the usefulness of this animal model to study viral determinants of lethality.

Two single mutations in the fusion protein of Newcastle disease virus confer hemagglutinin-neuraminidase independent fusion promotion and attenuate the pathogenicity in chickens.

The fusion (F) protein of Newcastle disease virus (NDV) affects viral infection and pathogenicity through mediating membrane fusion. Previously, we found NDV with increased fusogenic activity in which contained T458D or G459D mutation in the F protein. Here, we investigated the effects of these two mutations on viral infection, fusogenicity and pathogenicity. Syncytium formation assays indicated that T458D or G459D increased the F protein cleavage activity and enhanced cell fusion with or without the presence of HN protein. The T458D- or G459D-mutated NDV resulted in a decrease in virus replication or release from cells. The animal study showed that the pathogenicity of the mutated NDVs was attenuated in chickens. These results indicate that these two single mutations in F altered or diminished the requirement of HN for promoting membrane fusion. The increased fusogenic activity may disrupt the cellular machinery and consequently decrease the virus replication and pathogenicity in chickens.

Cyclooxygenase-2 promotes pulmonary intravascular macrophage accumulation by exacerbating BMP signaling in rat experimental hepatopulmonary syndrome.

One central factor in hepatopulmonary syndrome (HPS) pathogenesis is intravascular accumulation of activated macrophages in small pulmonary arteries. However, molecular mechanism underlying the macrophage accumulation in HPS is unknown. In this study, we aimed to explore whether elevated COX-2 induces the Bone morphogenic protein-2 (BMP-2)/Crossveinless-2 (CV-2) imbalance and then activation of BMP signaling pathway promotes the macrophage accumulation in Common Bile Duct Ligation (CBDL) rat lung.

Overview of Transgenic Mouse Models of Myeloproliferative Neoplasms (MPNs).

Myeloproliferative neoplasms (MPNs) are a class of hematologic diseases characterized by aberrant proliferation of one or more myeloid lineages and progressive bone marrow fibrosis. In 2005, seminal work by multiple groups identified the JAK2V617F mutation in a significant fraction of MPN patients. Since that time, murine models of JAK2V617F have greatly enhanced the understanding of the role of aberrant JAK-STAT signaling in MPN pathogenesis and have provided an in vivo pre-clinical platform that can be used to develop novel therapies. From early retroviral transduction models to transgenics, and ultimately conditional knock-ins, murine models have established that JAK2V617F alone can induce an MPN-like syndrome in vivo. However, additional mutations co-occur with JAK2V617F in MPNs, often in proteins involved in epigenetic regulation that can dramatically influence disease outcomes. In vivo modeling of these mutations in the context of JAK2V617F has provided additional insights into the role of epigenetic dysregulation in augmenting MPN hematopoiesis. In this overview, early murine model development of JAK2V617F is described, with an analysis of its effects on the hematopoietic stem/progenitor cell niche and interactions with downstream signaling elements. This is followed by a description of more recent in vivo models developed for evaluating the effect of concomitant mutations in epigenetic modifiers on MPN maintenance and progression. Mouse models of other driver mutations in MPNs, including primarily calreticulin (CALR) and Tpo-receptor (MPL), which occur in a significant percentage of MPN patients with wild-type JAK2, are also briefly reviewed. © 2017 by John Wiley & Sons, Inc.

A single amino acid change in the non-structural NV protein impacts the virulence phenotype of Viral hemorrhagic septicemia virus in trout.

Novirhabdoviruses like the Viral hemorrhagic septicemia virus (VHSV) are rhabdoviruses infecting fish. In the current study, RNA genomes of different VHSV field isolates classified as high, medium or low virulent phenotypes have been sequenced by next-generation sequencing and compared. Various amino acid changes, depending on the VHSV phenotype, have been identified in all the VHSV proteins. As a starting point, we focused our study on the non-virion (NV) non-structural protein in which an arginine residue (R116) is present in all the virulent isolates and replaced by a serine/asparagine residue S/N116 in the attenuated isolates. A recombinant virus derived from a virulent VHSV strain in which the NV R116 residue has been replaced by a serine, rVHSVNVR116S, was generated by reverse genetics and used to infect juvenile trout. We showed that rVHSVNVR116S was highly attenuated and that surviving fish were almost completely protected from a challenge with the wild-type VHSV.

Imbalance between innate antiviral and pro-inflammatory immune responses may contribute to different outcomes involving low- and highly pathogenic avian influenza H5N3 infections in chickens.

In order to gain further insight into the early virus-host interactions associated with highly pathogenic avian influenza virus infections in chickens, genome-wide expression profiling of chicken lung and brain was carried out at 24 and 72 h post-inoculation (h p.i.). For this purpose two recombinant H5N3 viruses were utilized, each possessing a polybasic HA0 cleavage site but differing in pathogenicity. The original rH5N3 P0 virus, which has a low-pathogenic phenotype, was passaged six times through chickens to give rise to the derivative rH5N3 P6 virus, which is highly pathogenic (Diederich S, Berhane Y, Embury-Hyatt C, Hisanaga T, Handel K et al.J Virol 2015;89:10724-10734). The gene-expression profiles in lung were similar for both viruses, although they varied in magnitude. While both viruses produced systemic infections, differences in clinical disease progression and viral tissue loads, particularly in brain, where loads of rH5N3 P6 were three orders of magnitude higher than rH5N3 P0 at 72 .p.i., were observed. Although genes associated with gene ontology (GO) categories INFα and INFβ biosynthesis, regulation of innate immune response, response to exogenous dsRNA, defence response to virus, positive regulation of NF-κB import into the nucleus and positive regulation of immune response were up-regulated in rH5N3 P0 and rH5N3 P6 brains, fold changes were higher for rH5N3 P6. The additional up-regulation of genes associated with cytokine production, inflammasome and leukocyte activation, and cell-cell adhesion detected in rH5N3 P6 versus rH5N3 P0 brains, suggested that the balance between antiviral and pro-inflammatory innate immune responses leading to acute CNS inflammation might explain the observed differences in pathogenicity.

Highly pathogenic avian influenza H5N1 clade and clade 2.3.4 viruses do not induce a clade-specific phenotype in mallard ducks.

Among the diverse clades of highly pathogenic avian influenza (HPAI) H5N1 viruses of the goose/Guangdong lineage, only a few have been able to spread across continents: clade 2.2 viruses spread from China to Europe and into Africa in 2005-2006, clade viruses spread from China to Eastern Europe in 2009-2010 and clade viruses of the H5Nx subtype spread from China to Europe and North America in 2014/2015. While the poultry trade and wild-bird migration have been implicated in the spread of HPAI H5N1 viruses, it has been proposed that robust virus-shedding by wild ducks in the absence of overt clinical signs may have contributed to the wider dissemination of the clade 2.2, and viruses. Here we determined the phenotype of two divergent viruses from clade, a clade that spread widely, and two divergent viruses from clade 2.3.4, a clade that was constrained to Southeast Asia, in young (ducklings) and adult (juvenile) mallard ducks. We found that the virus-shedding magnitude and duration, transmission pattern and pathogenicity of the viruses in young and adult mallard ducks were largely independent of the virus clade. A clade-specific pattern could only be detected in terms of cumulative virus shedding, which was higher with clade than with clade 2.3.4 viruses in juvenile mallards, but not in ducklings. The ability of clade A/common buzzard/Bulgaria/38 WB/2010-like viruses to spread cross-continentally may, therefore, have been strain-specific or independent of phenotype in wild ducks.

Comparative analysis of European bat lyssavirus 1 pathogenicity in the mouse model.

European bat lyssavirus 1 is responsible for most bat rabies cases in Europe. Although EBLV-1 isolates display a high degree of sequence identity, different sublineages exist. In individual isolates various insertions and deletions have been identified, with unknown impact on viral replication and pathogenicity. In order to assess whether different genetic features of EBLV-1 isolates correlate with phenotypic changes, different EBLV-1 variants were compared for pathogenicity in the mouse model. Groups of three mice were infected intracranially (i.c.) with 102 TCID50/ml and groups of six mice were infected intramuscularly (i.m.) with 105 TCID50/ml and 102 TCID50/ml as well as intranasally (i.n.) with 102 TCID50/ml. Significant differences in survival following i.m. inoculation with low doses as well as i.n. inoculation were observed. Also, striking variations in incubation periods following i.c. inoculation and i.m. inoculation with high doses were seen. Hereby, the clinical picture differed between general symptoms, spasms and aggressiveness depending on the inoculation route. Immunohistochemistry of mouse brains showed that the virus distribution in the brain depended on the inoculation route. In conclusion, different EBLV-1 isolates differ in pathogenicity indicating variation which is not reflected in studies of single isolates.

Evaluation of protective immunity induced by DNA vaccination with genes encoding Toxoplasma gondii GRA17 and GRA23 against acute toxoplasmosis in mice.

Toxoplasma gondii, an obligatory intracellular protozoan, can cause serious public health problems and economic losses worldwide. Two novel dense granule proteins (GRA17 and GRA23) were recently identified as T. gondii-secreted proteins which are localized to the parasitophorous vacuole membrane (PVM) and can mediate the movement of small molecules between the host cell and parasitophorous vacuole (PV). In the present study, we evaluated the protective immunity induced by DNA vaccination with genes encoding GRA17 and GRA23 against acute toxoplasmosis in mice. Eukaryotic expressing plasmids pVAX-TgGRA17 and pVAX-TgGRA23 were constructed. Then, BALB/c mice were intramuscularly immunized with pVAX-TgGRA17, pVAX-TgGRA23, or pVAX-TgGRA17 + pVAX-TgGRA23 followed by challenge infection with the highly virulent RH strain of T. gondii. The specific immune responses and protective efficacy against T. gondii were examined by cytokine and serum antibody measurements, lymphocyte proliferation assays, flow cytometry of lymphocytes and the survival time after challenge. Our results showed that mice immunized with pVAX-TgGRA17, pVAX-TgGRA23, or pVAX-TgGRA17 + pVAX-TgGRA23 induced specific humoral and cellular responses, with higher level of IgG antibody, increased levels of Th1-type cytokines IFN-γ and IL-12 (p70), and CD3(+)CD4(+)CD8(-) and CD3(+)CD8(+)CD4(-) T cells, as well as prolonged survival time (9.1 ± 0.32 days for pVAX-TgGRA17, 10.8 ± 0.79 days for pVAX-TgGRA23, and 12.6 ± 2.55 days for pVAX-TgGRA17 + pVAX-TgGRA23) compared to the blank control (7.11 ± 0.33 days), PBS control (7.22 ± 0.44 days), and pVAX I control (7.11 ± 0.33 days). These results demonstrated that both TgGRA17 and TgGRA23 are potential vaccine candidates, TgGRA23 has a better immunogenicity, and co-immunization of pVAX-TgGRA17 and pVAX-TgGRA23 induces better protective efficacy.

Precision in the design of an experimental study deflects the significance of proteinase-activated receptor 2 expression in scrapie-inoculated mice.

Proteinase-activated receptor 2 (PAR2) is suspected to modulate the pathogenesis of various neurodegenerative conditions. We previously described delayed onset of clinical symptoms and prolonged survival of PAR2-deficient mice after intracerebral inoculation with prions. Here we report the results from a refined blinded study that aimed to investigate the effects of PAR2 deletion on scrapie pathogenesis after peripheral infection. This study failed to confirm that PAR2 deficiency impacts on the length of the incubation period, with PAR2-/- and PAR2+/+ littermates developing scrapie at the same time. To clarify the discrepancy between the two observations, we repeated the intracerebral inoculation study while utilizing our refined protocol, which aimed to limit possible sources of experimental bias. The study again failed to confirm the significant effect of PAR2 expression on the course of prion infection. Our report emphasizes and discusses the importance of unbiased experimental design and the selection of proper genetic controls when using genetically altered animal models for prion pathogenesis studies.

Toll-like receptor (TLR)21 signalling-mediated antiviral response against avian influenza virus infection correlates with macrophage recruitment and nitric oxide production.

Cytosine-guanosinedeoxynucleotide (CpG) DNA can be used for the stimulation of the toll-like receptor (TLR)21 signalling pathway in avian species which ultimately leads to up-regulation of gene transcription for pro-inflammatory molecules including nitric oxide and recruitment of innate immune cells. The objective of this study was to determine the antiviral effect of NO, produced in response to in ovo delivery of CpG DNA, against avian influenza virus (AIV) infection. We found that when CpG DNA is delivered at embryo day (ED)18 in ovo and subsequently challenged with H4N6 AIV at ED19 pre-hatch and day 1 post-hatching, CpG DNA reduces H4N6 AIV replication associated with enhanced NO production and macrophage recruitment in lungs. In vitro, we showed that NO originating from macrophages is capable of eliciting an antiviral response against H4N6 AIV infection. This study provides insights into the mechanisms of CpG DNA-mediated antiviral response, particularly against AIV infection in avian species.

Evolutionary analysis of whole-genome sequences confirms inter-farm transmission of Aleutian mink disease virus.

Aleutian mink disease virus (AMDV) is a frequently encountered pathogen associated with mink farming. Previous phylogenetic analyses of AMDV have been based on shorter and more conserved parts of the genome, e.g. the partial NS1 gene. Such fragments are suitable for detection but are less useful for elucidating transmission pathways while sequencing entire viral genomes provides additional informative sites and often results in better-resolved phylogenies. We explore how whole-genome sequencing can benefit investigations of AMDV transmission by reconstructing the relationships between AMDV field samples from a Danish outbreak. We show that whole-genome phylogenies are much better resolved than those based on the partial NS1 gene sequences extracted from the same alignment. Well-resolved phylogenies contain more information about the underlying transmission trees and are useful for understanding the spread of a pathogen. In the main case investigated here, the transmission path suggested by the tree structure was supported by epidemiological data. The use of molecular clock models further improved tree resolution and provided time estimates for the viral ancestors consistent with the proposed direction of spread. It was however impossible to infer transmission pathways from the partial NS1 gene tree, since all samples from the case farms branched out from a single internal node. A sliding window analysis showed that there were no shorter genomic regions providing the same phylogenetic resolution as the entire genome. Altogether, these results suggest that phylogenetic analyses based on whole-genome sequencing taking into account sampling dates and epidemiological data is a promising set of tools for clarifying AMDV transmission.

Mycoplasma hyopneumoniae vaccination at or shortly before weaning under field conditions: a randomised efficacy trial.

This study assessed the efficacy of two different Mycoplasma hyopneumoniae vaccination programmes in relation to the time of weaning. Eight hundred and twenty-eight piglets were randomly divided into three groups: group V1 was vaccinated three days before weaning, group V2 at weaning (21 days of age) and group NV was left non-vaccinated. Vaccinations were performed using Ingelvac MycoFLEX. After the nursery period, 306 pigs were allocated to fattening unit (F1) and 501 pigs to a second unit (F2). Efficacy was evaluated using performance parameters and pneumonia lesions at slaughter. Statistically significant differences were obtained in F2 where group V1 had a higher average daily weight gain compared to groups V2 and NV for the entire study period (17 and 18 g/day, respectively) and the fattening period (26 and 36 g/day, respectively) (P<0.05). Considering respiratory disease scores for both fattening units, group V1 was the only group where coughing severity did not increase significantly between placement and the end of the fattening period (P>0.05). Between groups, there were no statistically significant differences for the average lung lesion scores (V1=3.44; V2=4.61; NV=4.55, P>0.05) and the prevalence of pneumonia (V1=35.0 per cent; V2=38.0 per cent; NV=41.4 per cent, P>0.05). Overall, vaccination against M hyopneumoniae before weaning provided numerically better performance than vaccination at weaning, but did not reach statistical significance. An influenza outbreak in F1 and the presence of coexisting mixed respiratory infections in both F1 and F2 could have possibly influenced the performance of both vaccinated groups across all measured parameters.

Molecular detection of Neospora caninum infection in ovine aborted foetuses in the Mashhad area, Iran

N. caninum could cause abortion in small ruminants. The aim of the study was to detect N. caninum infection in ovine aborted foetuses in the Mashhad area by PCR examination. During the period 2009 to 2013, 71 ovine aborted foetuses were collected and their brain samples examined by PCR. Of the 71 brains of the aborted foetuses, N. caninum DNA was detected in seven (9.8%) samples. In conclusion, it seems that N. caninum may act as a causative agent of abortion in sheep in the Mashhad area.

Intestinal and external parasites of raccoon dogs (Nyctereutes procyonoides) in western Poland

Parasites of an invasive species, the raccoon dog (Nyctereutes procyonoides) from western Poland were investigated to clarify poorly known ecological key aspects of the species. The research was conducted in two study areas: the Ujście Warty National Park and the Bogdaniec Forestry District. Intestinal samples were collected from the intestinal tracks of 39 dead animals and 51 faecal samples were collected in all seasons from latrines of raccoon dogs. Macro-parasites, their eggs and protozoan parasites were investigated to assess the taxonomic composition of parasites, the level of infection and the risk of potential transfer of dangerous parasites from raccoon dogs to people and native species. Among parasites potentially dangerous for human and native mammal species, Toxocara canis was found in the intestines and T. canis eggs, Cryptosporidium sp. oocysts and Entamoeba sp. cysts were identified in faecal samples. Sarcoptic mange was observed in the skin of two animals, whereas Diptera larvae (probably from the family Gasterophilidae) were found in the intestines of two other animals. This latter finding is very interesting, because Gasterophilidae are the typical parasites in horses and ungulates, but so far were never found in raccoon dogs.

Endoparasites of Eurasian lynx (Lynx lynx) (Linnaeus, 1758) from an enclosure of Western Pomeranian Nature Society in Jablonowo

The aim of this study was to describe parasites of three lynx living in an enclosure of Western Pomeranian Nature Society in Jablonowo. During analysis of 3 gram faecal samples eggs of Toxascaris leonina, Toxocara cati, Ancylostoma sp. and oocysts of Cystoisospora felis were found. To our knowledge this is the first report of C. felis infection in lynx from Poland. Presented research show that wild cats in captivity are particularly exposed on parasitic infections and demand regular examination.

Schmallenberg virus infection confirmed in Scotland.

Schmallenberg virus infection in malformed lambsFood chain issues after lead poisoning incidentSuspected ragwort poisoning in heifersEwe abortions due to Salmonella enterica serovar UrbanaCoxiella burnetii detected in aborted lambsThese are among matters discussed in the disease surveillance report for February 2017 from SAC Consulting: Veterinary Services (SAC C VS).

The performance of serological tests for Leishmania infantum infection screening in dogs depends on the prevalence of the disease.

Dogs are considered the main reservoir of Leishmania infantum. This protozoan causes visceral leishmaniasis (VL), an uncontrolled urban zoonosis in Brazil. Serological tests and polymerase chain reaction (PCR) on peripheral blood were performed to identify infected dogs in scenarios of higher and lower prevalence of the disease (Teresina and Vitória). One-hundred infected and 57 non-infected animals from Teresina and 100 non-infected animals from Vitória were studied. Animal selection was not dependent on previous serology. The sensitivity (Teresina) and specificity (Teresina and Vitória) were as follows: indirect antibody fluorescence (IFAT) cut-off of 1:40 (IFAT 1:40): 96%, 18%, and 76%; IFAT 1:80: 90%, 33%, and 93%; direct agglutination test (DAT): 96%, 33%, and 98%; fast agglutination screening test (FAST): 93%, 68%, and 100%; immunochromatographic assay with a recombinant rK39 antigen (rK39): 88%, 74%, and 98%; enzyme linked immunosorbent assay (ELISA): 91%, 79%, and 98%; rapid dual-path platform test (TR DPP®): 98%, 60%, and 98%; and blood PCR: 29%, 93%, and 97%, respectively. In the high transmission area, none of the tests adequately discriminated L. infantum-infected from non-infected dogs. However, in the high transmission city, the area under the receiver operating characteristic (ROC) curve of FAST, DAT, ICrK39, ELISA and TR DPP® was high.

Heterologous post-infection immunity against Egyptian avian influenza virus (AIV) H9N2 modulates the course of subsequent infection by highly pathogenic AIV H5N1, but vaccination immunity does not.

In Egypt, zoonotic A/goose/Guangdong/1/96 (gs/GD-like) highly pathogenic avian influenza virus (HPAIV) H5N1 of clade is entrenched in poultry populations and has co-circulated with low-pathogenic avian influenza virus H9N2 of the G1 lineage since 2010. Here, the impact of H9N2 infection or vaccination on the course of consecutive infection with a lethal Egyptian HPAIV H5N1 is studied. Three-week-old chickens were infected with H9N2 or vaccinated with inactivated H9N2 or H5N1 antigens and challenged three weeks later by an HPAIV H5N1. Interestingly, pre-infection of chickens with H9N2 decreased the oral excretion of H5N1 to levels that were comparable to those of H5N1-immunized chickens, but vaccination with inactivated H9N2 did not. H9N2 pre-infection modulated but did not conceal clinical disease by HPAIV H5N1. By contrast, homologous H5 vaccination abolished clinical syndromic surveillance, although vaccinated clinical healthy birds were capable of spreading the virus.

A porcine enterovirus G associated with enteric disease contains a novel papain-like cysteine protease.

Identification of unknown pathogens in pigs displaying enteric illness is difficult due to the large diversity of bacterial and viral species found within faecal samples. Current methods often require bacterial or viral isolation, or testing only a limited number of known species using quantitative PCR analysis. Herein, faeces from two 25-day-old piglets with diarrhoea from Texas, USA, were analysed by metagenomic next-generation sequencing to rapidly identify possible pathogens. Our analysis included a bioinformatics pipeline of rapid short-read classification and de novo genome assembly which resulted in the identification of a porcine enterovirus G (EV-G), a complete genome with substantial nucleotide differences (>30 %) among current sequences, and a novel non-structural protein similar in sequence to the Torovirus papain-like cysteine protease (PLpro). This discovery led to the identification and circulation of an EV-G with a novel PLpro in the USA that has not been previously reported.

Wildlife: topical issues, recent cases.

This focus article was prepared by Paul Duff, Paul Holmes and Alex Barlow of the APHA Wildlife Expert Group.