Benjamin Schade

Bone marrow depletion with haemorrhagic diathesis in calves in Germany: characterization of the disease and preliminary investigations on its aetiology.

Since 2007 a new fatal haemorrhagic diathesis in calves has been observed in all areas of Germany. Analysis of 56 cases submitted for necropsy allowed its characterization. Calves fell ill within the first month of life independent of breed and sex. Only single or a few animals per herd were affected. Petechial and ecchymotic haemorrhages in many organs and tissues, particularly in skin, subcutis and gastrointestinal tract, were major findings in all animals. Microscopically a severe depletion of bone marrow cells was always observed. Lymphocytic depletion (43%) and inflammatory lesions (46%) were less frequently observed. Blood analysis of five animals indicated an aplastic pancytopenia. The resulting thrombocytopenia is regarded as major pathomechanism of this Haemorrhagic Disease Syndrome (HDS). Pedigree analysis gave no indication of hereditary disease. Tests for specific toxins such as S-(1,2-Dichlorovinyl)-L-cysteine (DCVC), furazolidone, or mycotoxins resulting in bone marrow depletion were negative. Bacterial infections, Bovine Viral Diarrhoea Virus, and Bluetongue Virus were ruled out as cause of the disease. HDS shares similarities with a circoviral infection in chickens (chicken infectious anaemia). A broad-spectrum PCR allowed detection of circoviral DNA in 5 of 25 HDS cases and in 1 of 8 non-HDS cases submitted for necropsy. Sequencing of the whole viral genome revealed a high similarity (up to 99%) with Porcine Circovirus type 2b. Single bone marrow cells stained weakly positive for PCV2 antigen by immunohistochemistry in 1 of 8 tested HDS animals. This is the first report of circovirus detection in cattle in Germany. The exact cause of HDS still remains unknown. A multifactorial aetiology involving infection, poisoning, immunopathy, or a genetic predisposition is conceivable. Additional research is necessary to clarify the pathogenesis and the potential role of PCV2 in HDS.

Adenoviral Gizzard Erosion in Broiler Chickens in Germany

SUMMARY. 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. RESUMEN. Reporte de Caso—Erosión de la molleja por adenovirus en pollos en Alemania. Las infecciones por adenovirus aviar causan complejos importantes de enfermedad en pollos, pero muchos de estos virus también infectan a los pollos sin resultar en una enfermedad manifiesta. Se han reportado previamente en Japón varios brotes de erosiones en la molleja causadas por un adenovirus A del serotipo 1 (FAdV-1). Aquí se presenta un brote de erosiones en la molleja en 12 parvadas de pollos en Alemania en el 2011. Los pollos mostraron una reducción de la ganancia diaria de peso y un aumento en la tasa de mortalidad total de hasta 8%. Las aves mostraron un desprendimiento severo de la capa queratinizada y lesiones ulcerosas a necrotizantes de la mucosa subyacente. Histopatológicamente, se diagnosticó ventriculitis necrotizante con cuerpos de inclusión intranucleares basófilos en las células epiteliales. Mediante inmunohistoquímica, aislamiento viral y por el examen de microscopía electrónica se observaron partículas virales sugestivas de adenovirus en las muestras. No se pudo identificar algún agente infeccioso concurrente. Posteriormente, el virus se tipificó genéticamente como un FAdV-1 por PCR y por análisis de secuencias. El análisis filogenético de la asa L1 del hexón mostró un 100% de identidad con la secuencia con el virus CELO (chicken embryo lethal orphan). Estos hallazgos sugieren que los brotes de erosión de la molleja por adenovirus pueden ocasionar pérdidas económicas significativas en Alemania y pueden ser causados por una cepa virulenta inusual del FAdV-1.

Syndrome of arachnomelia in Simmental cattle

BackgroundThe syndrome of arachnomelia is an inherited malformation mainly of limbs, back and head in cattle. At present the arachnomelia syndrome has been well known mainly in Brown Swiss cattle. Nevertheless, the arachnomelia syndrome had been observed in the Hessian Simmental population during the decade 1964–1974. Recently, stillborn Simmental calves were observed having a morphology similar to the arachnomelia syndrome. The goal of this work was the characterization of the morphology and genealogy of the syndrome in Simmental to establish the basis for an effective management of the disease.ResultsThe first pathologically confirmed arachnomelia syndrome-cases in the current Simmental population appeared in the year 2005. By 2007, an additional 140 calves with the arachnomelia syndrome were identified. The major pathological findings were malformed bones affecting the head, long bones of the legs and the vertebral column. It could be shown that, with the exception of two cases that were considered as phenocopies, all of the paternal and about two-third of the maternal pedigrees of the affected calves could be traced back to one common founder. Together with the data from experimental matings, the pedigree data support an autosomal recessive mutation being the etiology of the arachnomelia syndrome. The frequency of the mutation in the current population was estimated to be 3.32%.ConclusionWe describe the repeated occurrence of the arachnomelia syndrome in Simmental calves. It resembles completely the same defect occurring in the Brown Swiss breed. The mutation became relatively widespread amongst the current population. Therefore, a control system has to be established and it is highly desirable to map the disease and develop a genetic test system.

Tick-borne encephalitis in a naturally infected sheep

BackgroundTick-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 presentationIn 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.ConclusionTo 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.

Prävalenz von Hilfsschleimbeuteln (Bursae auxiliares) und Klauenverletzungen bei Mastschweinen zum Schlachtzeitpunkt – Ergebnisse einer Studie an vier Schlachthöfen

The formation of auxiliary bursae is not part of the embryonal development but occurs as a pathologic reaction to a trauma, especially when exposed parts of the extremities are mechanically stressed. Among other reasons the keeping of pigs on artificial flooring and in particular the use of fully slatted flooring surfaces plays an important role.In a study at four abattoirs in Southern Germany we investigated the prevalence of auxiliary bursae in fattening pigs at the time of delivery and during meat inspection. For that purpose classification criteria were developed to record and graduate the occurrence and type of severity of bursae. Animals without appearance of bursae were graded 0, while animals with bursae being lightly, moderately or severely pronounced were graded 1, 2 and 3 respectively. 91.2% of 9 2 randomly selected finishers from conventional keeping showed prevalence of grade 1 to 3 bursae (grade 1: 7.7%; grade 2: 3. %; grade 3: 0.7 %), only 2.2% of these pigs were not affected (grade 0). In addition, claw injuries were detected in 26.5% of another group of 00 randomly selected fattening pigs.The prevalence of auxiliary bursae in a control group, consisting of 52 animals from organic production, was only 13.2%. In this group, the detected bursae were less pronounced (grade 1) and no claw injuries appeared.The high prevalence of technopathies such as auxiliary bursae and claw injuries in fattening pigs from conventional production points to the need for action regarding animal welfare and are relevant for operative selfmonitoring measurements based on the German animal protection law (§ 11). Information on the origin of the animals, i. e. on farms, was not available throughout the study because of privacy reasons. In order to investigate causal factors for the development of auxiliary bursae and claw injuries beyond the keeping of animals on fully slatted floors, a study on risk factors is necessary. Our data demonstrate that collection of animal welfare data collected at slaughter is needed as a base for veterinary guidance and onfarm interventions aiming to improve animal health and welfare standards.

Technopathies of the limbs in finishing pigs: risk factors, origin and impact on animal welfare

Ziel des vorliegenden ersten Teils dieser Untersuchung war, unter definierten Bedingungen die Entstehung und weitere Entwicklung akzessorischer Bursen an den Gliedmasen von Mastschweinen zu erfassen. Material und Methoden: 192 Masthybriden wurden von der Aufzucht bis zur Schlachtung unter konventionellen Haltungsbedingungen untersucht. Wochentlich wurden die Parameter Allgemeinbefinden, Anzahl, Grose und Lokalisation der akzessorischen Bursen an Gliedmasen und Sternum sowie Gang und Klauen erfasst. Ergebnisse: Akzessorische Bursen konnen an bis zu 13 Stellen an den Gliedmasen bzw. dem Sternum auftreten. Es wurden bereits Ferkel mit akzessorischen Bursen in die Aufzucht eingestallt, die Pravalenz stieg wahrend Aufzucht und Mast an und lag vor der Schlachtung bei 97,8 % der Tiere (Einstallung mit 4 Wochen: 25,5 %; Umstallung in die Mast mit 12 Wochen: 67,6 %). Schwere Tiere wiesen signifikant mehr und grosere Bursen auf als gleichaltrige leichtere Tiere. Auserdem nahmen sie grosere Futtermengen auf, riefen aber weniger haufig Futter ab. Tiere mit starkeren Gangbildveranderungen zeigten signifikant mehr und grosere Bursen. Am Schlachthof bestand bei 95,6 % der Tiere mindestens eine Klauenveranderung. Das Allgemeinbefinden wurde durch akzessorische Schleimbeutel nicht beeintrachtigt. Schlussfolgerung und klinische Relevanz: Eine Beeintrachtigung des Wohl-befindens hinsichtlich Schmerzempfinden durch akzessorische Bursen wird aufgrund der vorliegenden Ergebnisse und der Funktion als Schutzkissen nicht vermutet. Dennoch entstehen akzessorische Bursen in hoher Pravalenz und Anzahl pro Tier unter Einfluss verschiedener Faktoren erst im Laufe des Lebens und stellen eine Technopathie dar. Aufgrund der Exposition akzessorischer Bursen besteht das Risiko, dass diese sich infolge von Verletzungen zu eroffneten Grad-3-Bursen entwickeln.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.

Pseudomonas aeruginosa Infection in a Group of Captive Humboldt Penguins (Spheniscus humboldti)

Abstract Nine Humboldt penguins (Spheniscus humboldti), between 1 and 1.5 years old and kept at Zoo Dresden, developed local and systemic infections with various opportunistic pathogens within a period of 4 months. Affected birds died peracutely without preceding symptoms or showed various clinical signs, including separation from conspecifics, reduced food intake, lethargy, dyspnea, swelling of the salt glands, and ocular discharge. One bird showed central nervous signs, including seizures. Pathologic examination of deceased birds revealed severe necrotizing inflammation of the mucous membranes and deep structures of the glottis, trachea, nasal sinus, and conchae and granulomatous inflammation of the salt glands. Further findings were airsacculitis, pneumonia, hepatitis, conjunctivitis, and myositis. Pseudomonas aeruginosa was the predominant pathogen in 7 cases. Six penguins died or were euthanatized, whereas 3 penguins that received systemic antibiotic treatment with tobramycin (10 mg/kg IM q24h for 10 days) showed rapid clinical improvement. Insufficient turnover rate of the filtration system, biofilm formation on pipe surfaces, and other factors are assumed to have promoted pathogen buildup in the pool water and subsequent infection.