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1.
Avian Dis ; 66(1): 119-123, 2022 03.
Article En | MEDLINE | ID: mdl-35230044

Fowl glioma-inducing virus (FGV), a strain of avian leukosis virus (ALV) subgroup A, is the causal agent of fowl glioma characterized by multiple nodular astrocytic growths, gliosis, and lymphocytic encephalitis. Also associated with FGV infection are cases of cerebellar hypoplasia, perineuromas, and nonsuppurative myocarditis. Though fowl glioma has been recognized in several countries, most reports of FGV infection come from Japan. A 9-mo-old brown leghorn from a German farm with nine leghorns was presented to a veterinarian with an impaired general health with torticollis, tremor, and incoordination. Histopathology revealed multifocal nodular astrocytic growths, gliosis, and a lymphoplasmacytic encephalitis. Immunohistochemically, neoplastic astrocytes showed positivity for anti-ALV antibody. FGV was detected in the brain with nested reverse transcription-polymerase chain reaction (RT-PCR) and subsequent sequencing of PCR product. The remaining eight birds were screened for the presence of ALV with real-time RT-PCR. Four leghorns tested positive for exogenous ALV in nested RT-PCR with an identical nucleotide sequence as the leghorn with neurological symptoms. To the authors' knowledge this is the first report of a natural FGV infection in a brown leghorn in Germany with clinical manifestation.


Glioma aviar de manifestación clínica y natural en un pollo Leghorn en Alemania. El virus inductor del glioma del pollo (FGV), una cepa del subgrupo A del virus de la leucosis aviar (ALV), es el agente causal del glioma del pollo caracterizado por crecimientos astrocíticos nodulares múltiples, gliosis y encefalitis linfocítica. También se asocian con la infección por este virus, casos de hipoplasia cerebelar, perineuromas y miocarditis no supurativa. Aunque el glioma aviar se ha reconocido en varios países, la mayoría de los informes de infección por el virus inductor del glioma del pollo provienen de Japón. Un pollo Leghorn marrón de nueve meses de edad proveniente de una granja alemana con nueve aves Leghorns fue remitido a una clínica veterinaria con problemas de salud en general, tortícolis, temblores y falta de coordinación. La histopatología reveló crecimientos astrocíticos nodulares multifocales, gliosis y encefalitis linfoplasmocítica. Inmunohistoquímicamente, los astrocitos neoplásicos mostraron reacción positiva para anticuerpos contra el virus de la leucosis aviar. El virus inductor del glioma del pollo se detectó en el cerebro mediante transcripción reversa y reacción en cadena de la polimerasa anidada (RT-PCR) y con secuenciación posterior del producto de PCR. Las ocho aves restantes se examinaron para detectar la presencia del virus de la leucosis aviar mediante RT-PCR en tiempo real. Cuatro aves Leghorn dieron positivo para virus exógenos de leucosis mediante RT-PCR anidada y con una secuencia de nucleótidos idéntica a la del ave Leghorn con síntomas neurológicos. De acuerdo con el conocimiento de los autores, este es el primer informe de una infección natural por el virus inductor del glioma del pollo en un ave Leghorn marrón en Alemania que presentaba manifestaciones clínicas.


Avian Leukosis Virus , Avian Leukosis , Encephalitis , Glioma , Animals , Avian Leukosis/pathology , Chickens , Encephalitis/veterinary , Glioma/pathology , Glioma/veterinary , Gliosis/veterinary , Real-Time Polymerase Chain Reaction/veterinary
2.
Microorganisms ; 9(5)2021 May 14.
Article En | MEDLINE | ID: mdl-34069313

Viral diseases remain a major concern for animal health and global food production in modern agriculture. In chickens, avian leukosis virus subgroup J (ALV-J) represents an important pathogen that causes severe economic loss. Until now, no vaccine or antiviral drugs are available against ALV-J and strategies to combat this pathogen in commercial flocks are desperately needed. CRISPR/Cas9 targeted genome editing recently facilitated the generation of genetically modified chickens with a mutation of the chicken ALV-J receptor Na+/H+ exchanger type 1 (chNHE1). In this study, we provide evidence that this mutation protects a commercial chicken line (NHE1ΔW38) against the virulent ALV-J prototype strain HPRS-103. We demonstrate that replication of HPRS-103 is severely impaired in NHE1ΔW38 birds and that ALV-J-specific antigen is not detected in cloacal swabs at later time points. Consistently, infected NHE1ΔW38 chickens gained more weight compared to their non-transgenic counterparts (NHE1W38). Histopathology revealed that NHE1W38 chickens developed ALV-J typical pathology in various organs, while no pathological lesions were detected in NHE1ΔW38 chickens. Taken together, our data revealed that this mutation can render a commercial chicken line resistant to highly pathogenic ALV-J infection, which could aid in fighting this pathogen and improve animal health in the field.

3.
Oncogene ; 40(10): 1896-1908, 2021 03.
Article En | MEDLINE | ID: mdl-33603167

Recent years have seen an increasing number of genetically engineered pig models of human diseases including cancer. We previously generated pigs with a modified TP53 allele that carries a Cre-removable transcriptional stop signal in intron 1, and an oncogenic mutation TP53R167H (orthologous to human TP53R175H) in exon 5. Pigs with the unrecombined mutant allele (flTP53R167H) develop mainly osteosarcoma but also nephroblastomas and lymphomas. This observation suggested that TP53 gene dysfunction is itself the key initiator of bone tumorigenesis, but raises the question which aspects of the TP53 regulation lead to the development of such a narrow tumour spectrum. Molecular analysis of p53 revealed the presence of two internal TP53 promoters (Pint and P2) equivalent to those found in human. Consequently, both pig and human express TP53 isoforms. Data presented here strongly suggest that P2-driven expression of the mutant R167H-Δ152p53 isoform (equivalent to the human R175H-Δ160p53 isoform) and its circular counterpart circTP53 determine the tumour spectrum and play a critical role in the malignant transformation in flTP53R167H pigs. The detection of Δ152p53 isoform mRNA in serum is indicative of tumorigenesis. Furthermore, we showed a tissue-specific p53-dependent deregulation of the p63 and p73 isoforms in these tumours. This study highlights important species-specific differences in the transcriptional regulation of TP53. Considering the similarities of TP53 regulation between pig and human, these observations provide useful pointers for further investigation into isoform function including the novel circTP53 in both the pig model and human patients.


Carcinogenesis/genetics , Neoplasms/genetics , RNA, Circular/genetics , Tumor Suppressor Protein p53/genetics , Alleles , Animals , Disease Models, Animal , Exons/genetics , Gene Expression Regulation, Neoplastic/genetics , Humans , Introns/genetics , Neoplasms/pathology , Promoter Regions, Genetic/genetics , Protein Isoforms/genetics , Swine/genetics
4.
Article De | MEDLINE | ID: mdl-30340240

OBJECTIVE: The aim of the first part of the present study was to specify risk factors for the development of adventitious bursae on the limbs of weaning and finishing pigs. MATERIAL AND METHODS: In total, 192 pigs were examined weekly, recording the following parameters: general condition, number, size and localization of adventitious bursae on the limbs and sternum, gait and claws. RESULTS: Adventitious bursae can occur at 13 positions on the limbs or sternum. These adventitious bursae were already evident when pigs were moved to the nursery. The prevalence of adventitious bursae increased constantly from weaning to slaughter. At the age of 24 weeks, 97.8 % of all investigated pigs displayed adventitious bursae (aged 4 weeks: 25.5 %; aged 12 weeks: 67.6 %). Heavier pigs had significantly more and larger adventitious bursae than lighter pigs of the same age. Furthermore, heavier pigs retrieved feed from the automatic feeder less frequently but ate larger amounts each time. In addition, pigs with poorer gait displayed significantly more adventitious bursae. In 95.6 % of all investigated pigs, claw lesions were evident at slaughter. The general condition was unaffected by adventitious bursae. CONCLUSION AND CLINICAL RELEVANCE: Referring to the results of the present study and the general function of bursae protecting underlying structure against pressure, there is no indication that adventitious bursae affect the animal welfare in terms of the sensation of pain. Influenced by various factors, adventitious bursae develop with high prevalence and number per animal over the course of the life of pigs and can be described as a technopathy. Because of the exposure of adventitious bursae, there is a risk to become an ulcerated bursa of degree three in relation to injuries.


Animal Welfare , Bursitis/veterinary , Feeding Behavior/physiology , Sus scrofa/physiology , Swine Diseases/epidemiology , Animals , Behavior, Animal/physiology , Bursitis/epidemiology , Bursitis/physiopathology , Gait/physiology , Risk Factors , Swine , Swine Diseases/physiopathology
5.
BMC Vet Res ; 13(1): 267, 2017 Aug 22.
Article En | MEDLINE | ID: mdl-28830430

BACKGROUND: Tick-borne encephalitis (TBE) is the most important viral tick borne zoonosis in Europe. In Germany, about 250 human cases are registered annually, with the highest incidence reported in the last years coming from the federal states Bavaria and Baden-Wuerttemberg. In veterinary medicine, only sporadic cases in wild and domestic animals have been reported; however, a high number of wild and domestic animals have tested positive for the tick-borne encephalitis virus (TBEV) antibody. CASE PRESENTATION: In May 2015, a five-month-old lamb from a farm with 15 Merino Land sheep and offspring in Nersingen/Bavaria, a TBEV risk area, showed impaired general health with pyrexia and acute neurological signs. The sheep suffered from ataxia, torticollis, tremor, nystagmus, salivation and finally somnolence with inappetence and recumbency. After euthanasia, pathological, histopathological, immunohistochemical, bacteriological, parasitological and virological analyses were performed. Additionally, blood samples from the remaining, healthy sheep in the herd were taken for detection of TBEV antibody titres. At necropsy and accompanying parasitology, the sheep showed a moderate to severe infection with Trichostrongylids, Moniezia and Eimeria species. Histopathology revealed mild to moderate necrotising, lymphohistiocytic and granulocytic meningoencephalitis with gliosis and neuronophagia. Immunohistochemistry for TBEV was negative. RNA of a TBEV strain, closely related to the Kumlinge A52 strain, was detected in the brain by quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) and subsequent PCR product sequencing. A phylogenetic analysis revealed a close relationship to the TBEV of central Europe. TBEV was cultured from brain tissue. Serologically, one of blood samples from the other sheep in the herd was positive for TBEV in an enzyme-linked immunosorbent assay (ELISA) and in a serum neutralisation test (SNT), and one was borderline in an ELISA. CONCLUSION: To the authors' knowledge this is the first report of a natural TBEV infection in a sheep in Europe with clinical manifestation, which describes the clinical presentation and the histopathology of TBEV infection.


Encephalitis Viruses, Tick-Borne , Encephalitis, Tick-Borne/veterinary , Sheep Diseases/virology , Animals , Antibodies, Viral/blood , Brain/virology , Encephalitis Viruses, Tick-Borne/isolation & purification , Encephalitis, Tick-Borne/diagnosis , Sheep , Sheep Diseases/diagnosis
6.
Berl Munch Tierarztl Wochenschr ; 127(5-6): 183-7, 2014.
Article En | MEDLINE | ID: mdl-24881267

Erysipelas was diagnosed in a free-range laying flock with a high mortality of up to 7% per day and a severe decrease in egg production to 45%. The disease had a short course and unusual clinical features for erysipelas, including swollen, lacrimating and encrusted eyes. Bacteriologically, trapped poultry red mites and affected animals were culture-positive for Erysipelothrix rhusiopathiae. Isolates from layers and mites were both serotype 1b. Histopathology revealed disseminated intravasal coagulopathy in conjunctival small vessels as the cause of the oedema of the eye adnexes. After treatment with penicillin, mortality and egg production returned to normal levels. Although erysipelas in laying hens is rarely reported, it can develop as an emerging disease in alternative rearing systems and should always be considered if mortality increases in an older flock, especially with a high infestation of poultry red mites.


Chickens , Conjunctival Diseases/veterinary , Edema/veterinary , Erysipelas/veterinary , Poultry Diseases/epidemiology , Animals , Arachnid Vectors/microbiology , Conjunctival Diseases/microbiology , Disease Outbreaks/veterinary , Edema/microbiology , Erysipelas/complications , Erysipelas/epidemiology , Erysipelas/mortality , Erysipelothrix/isolation & purification , Female , Germany/epidemiology , Housing, Animal/legislation & jurisprudence , Housing, Animal/standards , Mites/microbiology , Oviposition , Poultry Diseases/microbiology , Poultry Diseases/mortality
7.
Avian Dis ; 57(1): 159-63, 2013 Mar.
Article En | MEDLINE | ID: mdl-23678748

Avian adenovirus infections cause important disease complexes in chickens, but many of the viruses also infect chickens without resulting in overt disease. Previously several outbreaks of gizzard erosions caused by a fowl adenovirus A serotype-1 (FAdV-1) were reported from Japan. Here we report an outbreak of gizzard erosions in 12 broiler flocks in Germany in 2011. Chickens had a reduced daily weight gain and a higher total mortality rate of up to 8%. The birds showed a severe detachment of the koilin layer and ulcerative to necrotizing lesions of the underlying mucosa. Histopathologically, necrotizing ventriculitis with basophilic, intranuclear inclusion bodies in epithelial cells was diagnosed. Immunohistochemistry, egg culture, and electron microscopic examination revealed adenovirus-like particles in the samples. No concurrent infectious agent could be identified. The virus was genotyped as FAdV-1 by PCR and subsequent sequencing. Phylogenetic analysis of the hexon loop L1 gene yielded 100% sequence identity to the chicken embryo lethal orphan strain. These findings suggest that outbreaks of adenoviral gizzard erosion can lead to significant economic losses in Germany and may be caused by an unusual virulent FAdV-1 strain.


Chickens , Disease Outbreaks/veterinary , Fowl adenovirus A/isolation & purification , Gizzard, Avian/pathology , Poultry Diseases/epidemiology , Poultry Diseases/virology , Stomach Diseases/veterinary , Animals , Capsid Proteins/genetics , Capsid Proteins/metabolism , Fowl adenovirus A/genetics , Genotyping Techniques/veterinary , Germany/epidemiology , Gizzard, Avian/ultrastructure , Microscopy, Electron, Transmission/veterinary , Phylogeny , Polymerase Chain Reaction/veterinary , Poultry Diseases/pathology , Sequence Analysis, DNA/veterinary , Stomach Diseases/epidemiology , Stomach Diseases/pathology , Stomach Diseases/virology , Weight Gain
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