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Schon fruh erkannte man, dass Viren bei Tieren Tumorerkrankungen hervorrufen konnen. Bereits 1911 beschrieb Peyton Rous, dass Viren bei Geflugel Sarkome verursachen. Das verantwortliche tumorauslosende Virus wurde spater nach ihm Rous-Sarkomvirus benannt. In den folgenden Jahrzehnten entdeckte man eine Vielzahl von Viren, die bei Geflugel und Nagetieren unterschiedliche Krebserkrankungen wie Lymphome, Sarkome und Karzinome auslosen konnen. Viele von ihnen gehoren zur Familie der Retroviridae und wurden den Gattungen der α-, β- und γ-Retroviren zugeordnet. Die Mehrzahl dieser Erreger wurde aus Inzuchtstammen der jeweiligen Tierarten oder aus Zellkulturen isoliert; unter naturlichen Bedingungen sind sie als Verursacher von Tumorerkrankungen der jeweiligen Tierarten wahrscheinlich ohne Bedeutung. Eine Ausnahme sind die Leukoseviren der Katze (FeLV; ▸Abschnitt 18.1). Das tumorerzeugende Potenzial der onkogenen Retroviren beruht auf transformationsaktiven Proteinen (v-Onc).

Retroviren wurden vor etwa 100 Jahren zum ersten Mal beschrieben: Nachdem Vilhelm Ellermann und Oluf Bang bereits 1908 die Mauseleukamie durch Ultrafiltrate ubertragen hatten, entdeckte Peyton Rous 1911, dass er mit ultrafiltrierten Extrakten aus Geflugelsarkomen diese Tumorerkrankung auf gesunde Huhner ubertragen konnte. Er erhielt hierfur 1966 den Nobelpreis, und das in den Extrakten enthaltene Retrovirus wurde nach ihm Rous-Sarkomvirus genannt. Einen weiteren Hinweis auf die Verursachung von Tumorerkrankungen durch Retroviren erhielt John J. Bittner 1936 bei seinen Untersuchungen zur Entstehung von malignen Milchdrusenerkrankungen der Maus: Er beschrieb das MMTV (Maus-Mammatumor-Virus) als den Erreger dieser Krankheit. Dieses Virus zeigte auch einen bis dahin unbekannten ubertragungsmodus: MMTV kann nicht nur als infektioses, von der Zelle freigesetztes, exogenes Partikel Ubertragen werden (horizontale ubertragung), sondern auch als endogener Bestandteil des Genoms von Keimbahnzellen auf die Folgegeneration (vertikale Ubertragung).

M. Hoskins sowie George M. Findlay und F. O. MacCallum entdeckten 1935 das Phanomen der Interferenz: Versuchstiere, die mit avirulenten Gelbfieberviren inokuliert wurden, erwiesen sich in den folgenden 24 Stunden vor Infektionen mit dem Wildtypvirus geschutzt. Die Ursache der Interferenz blieb lange Zeit unklar, bis 1957 Alick Isaacs und Jean Lindenmann in infizierten, bebruteten Huhnereiern die Substanz Interferon nachweisen konnten. Anfangs nahm man an, dass der durch Interferon vermittelte Abwehrmechanismus gegen „Fremdnucleinsauren“ gerichtet sei, da sich Interferon durch die doppelstrangige RNA der Reoviren effektiv induzieren lies. Seine Wirkungsweise war jedoch nicht sehr selektiv. Es zeigte sich bald, dass auch nichtinfizierte Zellen von Interferon beeinflusst werden und bei Verabreichung der Substanz an Tiere schwere Nebenwirkungen auftreten konnen. Zudem wurde klar, dass es im Organismus eine Basiskonzentration an Interferonen gibt, die physiologisch ist und durch haufige Virusinfektionen aufrechterhalten bleibt.

Bisher sind unter den human- und tierpathogenen Viren nur wenige bekannt, deren Genom als einzelstrangige DNA vorliegt: die Parvoviridae verfugen uber eine lineare, die Circoviridae und die erst kurzlich geschaffene Familie der Anelloviridae uber eine zirkular vorliegende Einzelstrang-DNA. Eine zirkulare, einzelstrangige DNA zeichnet auch die Geminiviridae aus, sie infizieren jedoch ausschlieslich Pflanzen. Circoviren sind virale Pathogene in Pflanzen und verschiedenen Tieren (Affen, Schweinen und Geflugel). 1997 konnte man erstmals ein zirkulares, einzelstrangiges DNA-Virus, das TT-Virus, aus dem Menschen isolieren. Es wird heute zu den Anelloviren gruppiert und persistiert ahnlich wie das etwas spater entdeckte TTM-Virus in den meisten Menschen und scheint keine Erkrankungen zu verursachen.

Viren sind infektiose Einheiten mit Durchmessern von etwa 16 nm (Circoviren) bis uber 300 nm (Pockenviren; ▸Tabelle 2.1). Ihre geringe Grose macht sie ultrafiltrierbar, das heist, sie werden durch bakteriendichte Filter nicht zuruckgehalten. Viren haben sich wahrend der Evolution in Millionen von Jahren entwickelt und an bestimmte Organismen beziehungsweise deren Zellen angepasst. Die infektiosen Viruspartikel oder Virionen bestehen aus Proteinen und sind bei einigen Virustypen von einer Lipidmembran umgeben, die man oft als Hulle oder Envelope bezeichnet; die Partikel enthalten jeweils nur eine Art von Nucleinsaure, namlich entweder DNA oder RNA. Viren vermehren sich nicht durch Teilung wie Bakterien, Hefen oder andere Zellen, sondern replizieren sich in lebenden Zellen, die sie infizieren. Dort entfalten sie ihre Genomaktiviat und produzieren die Komponenten, aus denen sie aufgebaut sind. Sie codieren weder fur eine eigene Proteinsynthesemaschinerie (Ribosomen) noch fur energiebildende Stoffwechselsysteme. Viren sind damit intrazellulare Parasiten. Open image in new window Molekularbiologische Charakteristika der verschiedenen Virusfamilien mit Angabe einiger typischer Vertreter

Viren sind aufgrund ihrer kurzen Generationszeit, der grosen Zahl von Nachkommen, die sie im Infektionsverlauf produzieren, und nicht zuletzt aufgrund ihrer einfachen Struktur ideale Objekte zum Studium von Evolutionsprozessen. Viren mussen sich standig den Bedingungen ihres Wirtes oder ihrer Wirtspopulationen anpassen, sodass Mechanismen der Selektion experimentellen Ansatzen zuganglich sind. Dabei spielen unterschiedliche Kriterien, wie die antigene Diversitat, das Ausmas der Virusausscheidung, der Grad der Virulenz und viele andere Faktoren eine wichtige Rolle. Die vollstandige Adaptation eines Virus an seinen Wirt, welche in eine moglichst geringe Virulenz des Infektionserregers mundet, ist die fur beide erstrebenswerte Konsequenz: ein problemloses Zusammen- und Uberleben. So scheinen die Hepatitis-G-Viren, die zwar erstmals aus Patienten mit einer Leberentzundung isoliert wurden, ahnlich wie die TT-Viren in vielen Menschen zu persistieren, ohne dass sie dabei Erkrankungen verursachen (▸Abschnitte 14.5 und 20.2).

Es sind viele Viren mit einem doppelstrangigen DNAGenom bekannt, die Saugetiere infizieren. Sie werden in sieben Virusfamilien eingeteilt: Hepadnaviridae, Polyomaviridae, Papillomaviridae, Adenoviridae, Herpesviridae, Poxviridae und Asfarviridae. Mit Ausnahme der Pox- und Asfarviridae hat man in allen Familien Vertreter gefunden, die in Menschen oder Tieren persistierende Infektionen herbeifuhren konnen. Hepadna-, Polyoma-,Papilloma- und Herpesviren stehen in enger kausaler Beziehung zu Tumorerkrankungen des Menschen. Dies legt nahe, dass Doppelstrang-DNA-Viren uber vielerlei Moglichkeiten verfugen, die Ablaufe der Zellteilung zu regulieren und zu beeinflussen. Die Hepadnaviren, die zu Beginn dieses Kapitels besprochen werden, stehen den Retroviren sehr nahe. Viele Details ihres Replikationszyklus weisen darauf hin, dass sie sich im Verlauf der Evolution aus den Retroviren entwickelt haben.

The demonstration of field isolates of porcine parvovirus (PPV) that differ genetically and antigenically from vaccine strains of PPV raises the question of whether the broadly used inactivated vaccines can still protect sows against the novel viruses. Ten specific-pathogen-free primiparous sows were assigned to three groups and were vaccinated with one of two vaccines based on the old vaccine strains, or served as non-vaccinated controls. After insemination, all sows were challenged with the prototype genotype 2 virus, PPV-27a, on gestation day 41; fetuses were delivered on gestation day 90 and examined for virus infection. The fetuses of the vaccinated sows were protected against disease, but both the vaccinated and the non-vaccinated sows showed a marked increase in antibody titres after challenge infection, indicating replication of the challenge virus. All sows (vaccinated and non-vaccinated) shed the challenge virus for at least 10 days after infection, with no difference in the pattern or duration of virus shedding.

Overview Avian influenza is a disease of birds, caused by a type A influenza virus. The subtype H5N1 avian influenza occurs primarily in birds and infection varies from mild disease with little or no mortality to a highly fatal, rapidly spreading epidemic (highly pathogenic avian influenza). It is extremely rare for cats to be infected and there are only very few confirmed reports of the disease in cats in Europe. Infection Cats can be infected via the respiratory and oral routes (eg, by eating infected birds). The key precondition for infection is that the cat lives in an area where H5N1 virus infection has been confirmed in birds. Additionally, the cat should have had outdoor access to an environment where waterfowl is present, or contact with poultry or uncooked poultry meat, or close contact with an H5N1-infected, sick cat during the first week of infection. Clinical suspicion Clinical signs in cats may include fever, lethargy, dyspnoea, conjunctivitis and rapid death. Neurological signs (circling, ataxia) have also been recorded. Diagnosis The veterinary authorities should be notified. Oropharyngeal, nasal and/or rectal swabs or faecal samples of suspected cases should be submitted for PCR and/or virus isolation. Post-mortem samples of lung and mediastinal lymph nodes should be obtained. Particular care should be taken when handling the cat and/or samples. Disease management The virus is sensitive to all standard medical disinfectants. Cats with suspected H5N1 infection should be kept in strict isolation. Owners should be advised to confine the cat to a separate room prior to bringing it to the veterinary clinic. Vaccination and disease prevention No H5N1 vaccines are commercially available for cats. In the event of confirmed cases of H5N1 avian influenza in birds in the area, owners should keep their cats indoors until further information is available, and follow official regulations.

Chlamydophila felis is a Gram-negative bacterium and its primary target is the conjunctiva. The bacterium does not survive outside the host.Transmission requires close contact between cats; ocular secretions are probably the most important body fluid for infection. Most cases occur in cats under 1 year of age. Chlamydophila felis is the infectious organism most frequently associated with conjunctivitis.Unilateral ocular disease generally progresses to become bilateral. There can be intense conjunctivitis with extreme hyperaemia of the nictitating membrane, blepharospasm and ocular discomfort. Transient fever, inappetence and weight loss may occur shortly after infection, although most cats remain well and continue to eat.PCR techniques are now preferred for diagnosing C felis infection. Ocular swabs are generally used. In unvaccinated cats, antibody detection can be used to indicate infection.Tetracyclines are generally regarded as the antibiotics of choice. Doxycycline has the advantage of requiring only single daily administration and is given at a dose of 10 mg/kg orally. Vaccination should be considered if there is a history of confirmed chlamydial disease in a shelter. Single housing and routine hygiene measures should suffice to avoid cross-infection. Cats maintained together for longer terms should be vaccinated regularly. In breeding catteries where C felis infection is endemic, the first step should be to treat all cats with doxycycline for at least 4 weeks. Once clinical signs have been controlled, the cats should be vaccinated.Vaccination should be considered for cats at risk of exposure to infection. Vaccination generally begins at 8-10 weeks of age, with a second injection 3-4 weeks later. Annual boosters are recommended for cats at continued risk of exposure.

Overview Feline immunodeficiency virus (FIV) is a retrovirus closely related to human immunodeficiency virus. Most felids are susceptible to FIV, but humans are not. Feline immunodeficiency virus is endemic in domestic cat populations worldwide. The virus loses infectivity quickly outside the host and is susceptible to all disinfectants. Infection Feline immunodeficiency virus is transmitted via bites. The risk of transmission is low in households with socially well-adapted cats. Transmission from mother to kittens may occur, especially if the queen is undergoing an acute infection. Cats with FIV are persistently infected in spite of their ability to mount antibody and cell-mediated immune responses. Disease signs Infected cats generally remain free of clinical signs for several years, and some cats never develop disease, depending on the infecting isolate. Most clinical signs are the consequence of immunodeficiency and secondary infection. Typical manifestations are chronic gingivostomatitis, chronic rhinitis, lymphadenopathy, weight loss and immune-mediated glomerulonephritis. Diagnosis Positive in-practice ELISA results obtained in a low-prevalence or low-risk population should always be confirmed by a laboratory. Western blot is the ‘gold standard’ laboratory test for FIV serology. PCR-based assays vary in performance. Disease management Cats should never be euthanased solely on the basis of an FIV-positive test result. Cats infected with FIV may live as long as uninfected cats, with appropriate management. Asymptomatic FIV-infected cats should be neutered to avoid fighting and virus transmission. Infected cats should receive regular veterinary health checks. They can be housed in the same ward as other patients, but should be kept in individual cages. Vaccination recommendations At present, there is no FIV vaccine commercially available in Europe. Potential benefits and risks of vaccinating FIV-infected cats should be assessed on an individual cat basis. Needles and surgical instruments used on FIV-positive cats may transmit the virus to other cats, so strict hygiene is essential.

Overview Feline leukaemia virus (FeLV) is a retrovirus that may induce depression of the immune system, anaemia and/or lymphoma. Over the past 25 years, the prevalence of FeLV infection has decreased considerably, thanks both to reliable tests for the identification of viraemic carriers and to effective vaccines. Infection Transmission between cats occurs mainly through friendly contacts, but also through biting. In large groups of non-vaccinated cats, around 30–40% will develop persistent viraemia, 30–40% show transient viraemia and 20–30% seroconvert. Young kittens are especially susceptible to FeLV infection. Disease signs The most common signs of persistent FeLV viraemia are immune suppression, anaemia and lymphoma. Less common signs are immune-mediated disease, chronic enteritis, reproductive disorders and peripheral neuropathies. Most persistently viraemic cats die within 2–3 years. Diagnosis In low-prevalence areas there may be a risk of false-positive results; a doubtful positive test result in a healthy cat should therefore be confirmed, preferably by PCR for provirus. Asymptomatic FeLV-positive cats should be retested. Disease management Supportive therapy and good nursing care are required. Secondary infections should be treated promptly. Cats infected with FeLV should remain indoors. Vaccination against common pathogens should be maintained. Inactivated vaccines are recommended. The virus does not survive for long outside the host. Vaccination recommendations All cats with an uncertain FeLV status should be tested prior to vaccination. All healthy cats at potential risk of exposure should be vaccinated against FeLV. Kittens should be vaccinated at 8–9 weeks of age, with a second vaccination at 12 weeks, followed by a booster 1 year later. The ABCD suggests that, in cats older than 3–4 years of age, a booster every 2–3 years suffices, in view of the significantly lower susceptibility of older cats.

Bordetella bronchiseptica is a Gram-negative bacterium that colonises the respiratory tract of mammals and is considered to be a primary pathogen of domestic cats. It is sensible to consider B bronchiseptica as a rare cause of zoonotic infections. The bacterium is susceptible to common disinfectants.The bacterium is shed in oral and nasal secretions of infected cats. Dogs with respiratory disease are an infection risk for cats. The microorganism colonises the ciliated epithelium of the respiratory tract of the host, establishing chronic infections.A wide range of respiratory signs has been associated with B bronchiseptica infection, from a mild illness with fever, coughing, sneezing, ocular discharge and lymphadenopathy to severe pneumonia with dyspnoea, cyanosis and death.Bacterial culture and PCR lack sensitivity. Samples for isolation can be obtained from the oropharynx (swabs) or via transtracheal wash/ bronchoalveolar lavage.Antibacterial therapy is indicated, even if the signs are mild. Where sensitivity data are unavailable, tetracyclines are recommended. Doxycycline is the antimicrobial of choice. Cats with severe B bronchiseptica infection require supportive therapy and intensive nursing care.In some European countries an intranasal modified-live virus vaccine is available. The modified-live product is licensed for use as a single vaccination with annual boosters. Cats should not be routinely vaccinated against B bronchiseptica (non-core), since the infection generally causes only a mild disease.

OVERVIEW: Rabies virus belongs to the genus Lyssavirus, together with European bat lyssaviruses 1 and 2. In clinical practice, rabies virus is easily inactivated by detergent-based disinfectants. INFECTION: Rabid animals are the only source of infection. Virus is shed in the saliva some days before the onset of clinical signs and transmitted through a bite or a scratch to the skin or mucous membranes. The average incubation period in cats is 2 months, but may vary from 2 weeks to several months, or even years. DISEASE SIGNS: Any unexplained aggressive behaviour or sudden behavioural change in cats must be considered suspicious. Two disease manifestations have been identified in cats: the furious and the dumb form. Death occurs after a clinical course of 1-10 days. DIAGNOSIS: A definitive rabies diagnosis is obtained by post-mortem laboratory investigation. However, serological tests are used for post-vaccinal control, especially in the context of international movements. DISEASE MANAGEMENT: Post-exposure vaccination of cats depends on the national public health regulations, and is forbidden in many countries. VACCINATION RECOMMENDATIONS: A single rabies vaccination induces a long-lasting immunity. Kittens should be vaccinated at 12-16 weeks of age to avoid interference from maternally derived antibodies and revaccinated 1 year later. Although some vaccines protect against virulent rabies virus challenge for 3 years or more, national or local legislation may call for annual boosters.

Overview Feline viral rhinotracheitis, caused by feline herpesvirus (FHV), is an upper respiratory tract disease that is often associated with feline calicivirus and bacteria. In most cats, FHV remains latent after recovery, and they become lifelong virus carriers. Stress or corticosteroid treatment may lead to virus reactivation and shedding in oronasal and conjunctival secretions. Infection Sick cats shed FHV in oral, nasal and conjunctival secretions; shedding may last for 3 weeks. Infection requires direct contact with a shedding cat. Disease signs Feline herpesvirus infections cause acute rhinitis and conjunctivitis, usually accompanied by fever, depression and anorexia. Affected cats may also develop typical ulcerative, dendritic keratitis. Diagnosis Samples consist of conjunctival, corneal or oropharyngeal swabs, corneal scrapings or biopsies. It is not recommended that cats recently vaccinated with a modified-live virus vaccine are sampled. Positive PCR results should be interpreted with caution, as they may be produced by low-level shedding or viral latency. Disease management ‘Tender loving care’ from the owner, supportive therapy and good nursing are essential. Anorexic cats should be fed blended, highly palatable food – warmed up if required. Mucolytic drugs (eg, bromhexine) or nebulisation with saline may offer relief. Broad-spectrum antibiotics should be given to prevent secondary bacterial infections. Topical antiviral drugs may be used for the treatment of acute FHV ocular disease. The virus is labile and susceptible to most disinfectants, antiseptics and detergents. Vaccination recommendations Two injections, at 9 and 12 weeks of age, are recommended, with a first booster 1 year later. Boosters should be given annually to at-risk cats. For cats in low-risk situations (eg, indoor-only cats), 3-yearly intervals suffice. Cats that have recovered from FHV-associated disease are usually not protected for life against further disease episodes; vaccination of recovered cats is therefore recommended.

In humans, herpes simplex virus type-1 has recently been detected in the vestibular ganglion (VG) and labyrinth (VL) and may be associated with vestibular signs. Feline herpesvirus-1 (FHV-1) is widespread amongst cat populations and affects many different tissues. The aim of this pilot study was to investigate the presence of FHV-1 DNA in the VG and VL of randomly selected domestic cats using PCR. FHV-1 DNA was detected in the VG of 14% of the cats. There was no detectable FHV-1 DNA in the VL of any cat. None of the infected cats had vestibular signs related to the VG infection.

The recently discovered human Bocavirus has been preliminary classified into the genus Bocavirus of the family Parvoviridae. Animal bocaviruses have been known in veterinary medicine since the early 1960s. This paper reviews the current knowledge about the two eponymous members of the genus: bovine parvovirus (BPV) and canine minute virus (CnMV). In contrast to other parvoviruses, bocaviruses contain a third open reading frame in the mid of the genome encoding for a highly phosphorylated non-structural protein, NP1, whose function has not yet been determined. The VP1-unique region of BPV and CnMV contains a phospholipase A2 sequence motif. Both viruses cause diseases of the gastrointestinal and respiratory tract and are known to infect fetuses and to cause reproductive disorders. Especially young animals suffer from disease, whereas in adults subclinical infection is common. Clinical signs include diarrhea, vomiting, dyspnea, embryonic/fetal death after transplacental infection early and abortion late in gestation. Both viruses have in common that they are widespread in their host species as worldwide serosurveys indicate. For BPV it has been shown that sialated glycoproteins mediate hemagglutination reaction and function as receptor for virus attachment on permissive cells.

In-house tests for the identification of faecal parvovirus antigen are now available. The majority of these are licensed for canine parvovirus only; but anecdotal information suggests that they will detect feline panleukopenia virus (FPV) as well. This prospective study was designed to compare five commercially available test systems. In total, 200 faecal samples from randomly selected healthy cats (148) and cats with diarrhoea (52) were tested and compared with the results of examination by electron microscopy. Ten cats were positive for FPV and all of these had diarrhoea. In-house canine parvovirus tests can be used to detect FPV. All tests were suitable to screen cats for faecal parvovirus excretion (positive predictive values for the Witness Parvo, the Snap Parvo, the SAS Parvo, the Fastest Parvo Strip, and the Speed Parvo were 100.0, 100.0, 57.1, 38.9, and 100%, respectively, negative predictive values for the Witness Parvo, the Snap Parvo, the SAS Parvo, the Fastest Parvo Strip, and the Speed Parvo were 97.4, 97.9, 98.9, 98.4, and 97.4%, respectively). In-house parvovirus tests may be positive up to 2 weeks after vaccination, and therefore, in recently vaccinated cats positive results do not necessarily mean infection.

Canine parvovirus (CPV), which causes hemorrhagic enteritis in dogs, has 3 antigenic variants: types 2a, 2b, and 2c. Molecular method assessment of the distribution of the CPV variants in Europe showed that the new variant CPV-2c is widespread in Europe and that the viruses are distributed in different countries.

Summary The efficacy of a homologous vaccination in preventing infection of suckling piglets with Salmonella (S.) Typhimurium was evaluated after an immunization of pregnant sows using an inactivated herd-specific S. Typhimurium vaccine. Twenty-five pregnant sows were vaccinated three times antepartum. The efficiency of this vaccine regime was assessed by comparison with a control group of 37 sows and their suckling piglets, which were daily treated with enrofloxacin from day 14 antepartum until the day of weaning. From the first day of life until day 142 post-partum, faecal samples of the piglets were collected and analysed for Salmonella shedding. In parallel, systemic antibody responses were monitored using a whole cell-based isotype-specific enzyme-linked immunosorbent assay (ELISA). The bacteriological investigation showed marked effects of vaccination. Salmonella Typhimurium could not be detected in any of the faecal samples of the piglets from the vaccinated sows. In contrast, the piglets of the group with long-time antibiotic treatment shed salmonellae rating to 47.4% of the animals. Furthermore, the offspring from vaccinated sows showed significantly decreased antibody activities of immunoglobulin (Ig)A and IgG. These bacteriological and serological results indicate a significantly lower Salmonella prevalence in piglets of the vaccinated group. As this study shows, the presented strategy of vaccination of pregnant sows with an inactivated Salmonella vaccine seems to be a suitable measure in decreasing Salmonella prevalence in offspring of infected sows.

Porcine reproductive and respiratory syndrome virus (PRRSV) is a major pathogen of swine. Due to genetic variation between the European and the US genotype as well as within both genotypes detection of PRRSV is a diagnostic challenge. This paper reports on a ring test to compare different established reverse transcriptase polymerase chain reaction methods applied routinely in 16 different laboratories in Germany. Three different sets of samples were sent to the laboratories which were to be analysed as follows: (i) basis package: detection of PRRS (yes/no); (ii) differentiation package I: differentiation of EU and US genotypes; and (iii) differentiation package II: differentiation of EU field isolates and EU vaccine strain. A total of 80% of the samples of the basic package were analysed correctly, the analysis of the differentiation package I revealed 61.82% correctly tested samples and the two laboratories that analysed the differentiation package II showed only one correct result. The ring test showed that the majority of incorrect diagnoses were false-negative results.

Oncogenic viruses are important pathogens in farm and companion animals. These original pathogens are classified in various virus families, such as Retroviridae, Papillomaviridae, and Herpesviridae. Besides a role as pathogens for its original host, animal viruses serve as valuable models for viruses affecting humans, such as hepatitis B virus, and issues of immunity, therapy, but also basic pathophysiological mechanisms, can often only be addressed in those animal systems.

Oncogenic viruses are important pathogens in farm and companion animals. These original pathogens are classified in various virus families, such as Retroviridae, Papillomaviridae, and Herpesviridae. Besides a role as pathogens for its original host, animal viruses serve as valuable models for viruses affecting humans, such as hepatitis B virus, and issues of immunity, therapy, but also basic pathophysiological mechanisms, can often only be addressed in those animal systems.

Yersiniosis is considered to be an emerging infection in humans. It is believed that contaminated pork is the main source of infection for man but also beef and cow milk might cause infection in the consumer. Therefore, a survey was carried out to obtain actual data on the prevalence of anti-Yersinia antibodies within cattle. 600 serum samples were taken form 120 farms located in 43 districts of Bavaria, Germany. Antibodies were detected in 396 animals (65.7%) revealing a distribution of 52.3% of anti-YopD, 40.3% of anti-YopM, 24.0% of anti-YopH, 21.2% of anti-YopE and 3.0% of anti-V-antigen antibodies. 21 reactionpatterns out of 32 possible patterns were identified. Anti-YopD and YopM antibodies were sufficient to detect all Yersinia antibody positive sera. No regional differences in the distribution of antibodies were noted.

Identification of bovine and ovine tissue from the central nervous system (CNS: brain and spinal cord) in meat products is possible by using certain CNS fatty acids as biomarkers in GC-MS analysis. Furthermore, the relationship between the isomers of the tetracosenic acid (C24:1) is important for differentiation of the species and age of the CNS in view of the legal definition of specified risk material (SRM). This has so far been referred to as the "cis/trans ratio of the isomers of nervonic acid"; however, structural analysis was not performed. Here we present results from GC-MS structural analysis by retention time and DMDS adduct profiling of the even numbered monoenoic fatty acids from C18:1 to C26:1. Retention times and mass spectra of the FAME standards indicated that the so far designated trans-nervonic acid has a different isomeric structure in the tetracosenic acid from brain-sample extracts. By performing GC-MS analysis of DMDS adducts we have shown that this isomer was actually cis-17-tetracosenic acid in all species so far tested, not trans-15-tetracosenic acid ( trans-nervonic acid). The tetracosenic acid isomer ratio proved to be species-specific in accordance with previous results. Thus, instead of the ratio of cis/trans isomers of nervonic acid, the ratio of omega 9/omega 7-tetracosenic acid (15c-C24:1/17c-C24:1) will have to be used as a correct reference in future publications. Although trans isomers were not detectable in sheep and cattle brain, porcine brain contained, in addition to cis-17-tetracosenic acid, small amounts of the trans isomers of the C18:1, C20:1, C24:1, and C26:1 fatty acids, in decreasing quantities. In future, this might be useful as another means of differentiation between porcine CNS (non-SRM) and ovine or bovine CNS (SRM). Extensive follow-up studies must be performed to elucidate the extent to which this GC-MS approach will facilitate the detection of CNS according to the legal SRM definition.

The potency to protect pigs against colonization and against clinical salmonellosis was evaluated after oral immunization with a live gyrA-cpxA-rpoB Salmonella (S.) Typhimurium mutant (S. Tm. Nal2/Rif9/Rtt). Twenty 4-week-old male hybrid piglets were immunized orally, a control group received a placebo. Three weeks postimmunization, all pigs were challenged orally with a highly virulent S. Typhimurium DT104 strain. Clinical investigation revealed that immunization prevented the vaccinated pigs from clinical symptoms of salmonellosis. While all placebo-treated animals showed a 2-4-day episode of moderate to severe clinical symptoms, 90% of immunized pigs did not show any clinical signs at all. The bacteriological results showed a marked beneficial effect of the oral immunization. Vaccinated pigs showed a significantly decreased rate of colonization of the inner organs (42.5% versus 87.5%) when compared to the placebo-treated animals. Furthermore, in comparison to the non-immunized pigs, the vaccines developed a higher specific immunoglobulin (Ig)A antibody activity, but a significant lower IgM antibody activity in serum. The findings underline the ability of an attenuated oral live S. Typhimurium mutant to prevent clinical symptoms of salmonellosis in pigs and to significantly reduce the colonization of tissues and inner organs, as well as the shedding of S. Typhimurium.

Canine parvovirus (CPV) evolved as a new pathogen in dogs between 1976 and 1978 from feline panleukopenia virus (FPV). The new virus hit an unprotected population, caused a dramatic pandemic and infected virtually all populations of domestic and wild carnivores worldwide. The great similarity between the two viruses and their differences in host range, both in vivo as well as in vitro, make it a good model system for emerging diseases and host range shifts of viruses. Recent results showed that CPV expanded its host range by binding to the canine transferrin receptor (Tfr). Residues in the capsid protein that had been defined as host range controlling regions also control the binding to the canine transferrin receptor. These residues are located on a raised region of the capsid at the three-fold axis of symmetry. Interestingly, adaption of the new virus to the new host appears to correlate with an improved binding to the Tfr receptor.

The aim of the present study was to provide current data on the prevalence of anti-Yersinia-antibodies in Bavarian slaughtering pigs. The recomBlot Westernblot assay based on five recombinantly produced Yersinia Outer Proteins (YopD, YopE, YopH, YopM, V-antigen) is well evaluated for the use in the diagnosis of human yersiniosis and proved to be also a valuable tool for the detection of porcine antibodies. 965 out of 1002 meat juice samples collected in 53 Bavarian pig farms contained anti-Yop/V-Ag-antibodies. Only blots with three or more detectable signals were considered as positive. On the basis of these results a possible previous history of Yersinia infection was detected in 45.4% of the pigs and all of the pig farms. The high prevalence of anti-Yersinia-antibodies found in this investigation demonstrates the need for further epidemiological surveillance and animal studies to assess consumers' endangering.

Summary Foamy viruses (FV) are complex retroviruses which are commonly isolated from cats, cattle and non-human primates. The infection is persistent and infected animals have a sustained antibody response. The role of FV in diseases remains unclear, in cats, a possible association with uncharacterized renal symptoms remains to be confirmed. To demonstrate feline FV (FFV) in tissues of experimentally infected cats three polyclonal monospecific antisera from rabbits against three different viral proteins, the structural Gag and the non-structural Bel 1 and Bet proteins were tested for their applicability in immunohistochemistry with paraffin sections. Only the Bet antiserum allowed detection of FFV-specific proteins, the antibodies against Gag and Bel 1 did not work even after pre-treatment of the slides with proteinase K or cooking in a pressure cooking pot. The Bet-reactive antibodies were detected using a commercial streptavidin kit and revealed Bet in the cytoplasm of cells from different lymphoid tissues like lymphnodes, tonsils, thymus and spleen. The method described opens new ways to explore the in vivo replication and tissue specificity of FFV and its possible role in disease.

The correlation between parvovirus infections and lesions in the central nervous system other than cerebellar hypoplasia was studied in 100 cats. The animals were necropsied with a history of various diseases, one third showing typical clinical and pathomorphological signs of panleukopenia. In 18 cats polyclonal antiserum against canine parvovirus consistently labeled neurons mainly in diencephalic regions, whereas the cerebellar cortex remained negative in all cases. In situ hybridization with digoxigenin-labeled minus-sense RNA probes, hybridizing with monomer-replicative form DNA or mRNA, revealed positive signals in nuclei of several neurons of the brain, again excluding the cerebellum. PCR applied to formalin-fixed and paraffin-embedded brain tissue and intestinal tissues of the diseased cats and subsequent DNA sequence analysis yielded canine parvovirus type 2 (CPV-2)-like sequences in the central nervous system. Two aspects of these findings are intriguing: (i) parvoviruses appear to be capable of replicating in neurons, cells that are considered to be terminally differentiated and (ii) CPV-like viruses of the old antigenic type CPV-2 appear to be able to infect cats.

In order to define the potential and applicability of replication-competent foamy virus-based vaccine vectors, recombinant feline foamy virus (FFV) vectors encoding defined segments of the feline calicivirus (FCV) capsid protein E domain were constructed. In cell cultures, these FFV-FCV vectors efficiently transduced and expressed a hybrid fusion protein consisting of the essential FFV Bet protein and the attached FCV E domains. The stability of the vectors in vitro was inversely correlated to the size of the heterologous insert. The deletion of a part of the FFV U3 sequence in these FFV-FCV vectors did not interfere with replication and titer in cell cultures but increased the genetic stability of the hybrid vectors. Selected chimeric vectors were injected into immunocompetent cats and persisted in the transduced host concomitant with a strong and specific humoral immune response against vector components. In a substantial number of cats, antibodies directed against the FCV E domain were induced by the FFV-FCV vectors, but no FCV-neutralizing activities were detectable in vitro. When the vaccinated cats were challenged with a high-titer FCV dose, sterile immunity was not induced by any of the hybrid FFV-FCV vectors. However, the FFV-FCV vector with a truncated U3 region of the long terminal repeat promoter significantly reduced the duration of FCV shedding after challenge and suppressed the appearance of FCV-specific ulcers. Possible mechanisms contributing to the partial protection will be discussed.

A total of 2754 bovine blood samples were examined for BHV1 antibodies in three different BHV-1 ELISA tests. The tests used were the CHEKIT Trachitest 2nd. Gen. "Bestätigungstest" Serum, the CHEKIT-BHV-1-gB-ELISA (Bommeli-Diagnostics/Intervet), and the BHV-1-gB Antibody Test Kit (IDEXX). A first testing identified 111 (4.0%) of the samples as positive and 2501 (90.8%) samples negative in all three tests. Onehundredand-fortytwo (5.2%) of the samples showed a not negative result in at least one of the two gB-ELISAs. The testing was repeated for 139 of the 142 samples and still 89 (3.2%) samples were found with discrepant results. The remaining 50 samples showed a negative reaction in the three ELISA tests. After Western blot analysis antibodies against glycoprotein B (gB) of BHV-1 were only detected in 11 of the 89 samples with a not negative reaction in at least one of the gB-ELISAs. Three of the 50 ELISA-negative samples showed a positive reaction in the Western blot. The high number of positive results in the gB-ELISAs which were negative in the Western blot assay leads to the conclusion that gB-ELISAs may have a lower specificity as the indirect ELISA. Introducing the gB-ELISA as the standard test for BHV1 serology in Bavaria would result to an increase of the number of BHV-1 positive farms by 8% (gB IDEXX) or 20% (gB Bommeli) 20%.

In Bavaria a BHV-1 eradication program was initiated in 1986 and was changed to a compulsory program in 1998. The eradication success increased progressively from50% in 1986 to 87% of the farms in 2002. BHV 1-free farms are controlled by bulk milk serology twice a year along with blood serology in animals that are negative but from herds where positive field virus infected animals are present. All serological tests are performed with an indirect ELISA test, all positive results are confirmed by a gB ELISA. Currently about 100.000 virus infected cattle are in Bavarian herds, approximately 80% of these animals are in heavily infected herds (10 infected animals). These herds comprise about 5% of all Bavarian herds. The eradication of the virus in these heavily infected herds is the most diifficult, whereas the prevention of new infections appears controllable. In this review current problems in BHV1 eradication are named and possible improvements are discussed.

A commercial ELISA detecting antibodies against bovine viral diarrhoea Virus (BVDV) was analysed for its applicability for bulk-milk screening. Detection limits were analysed using native and concentrated milk samples (milk treated with rennet and ammonium sulfate precipitated) from 10 cows whose sera showed different reactivity levels in the ELISA and from two cows which gave birth to persistently infected calves during the last year. Further this and a second commercial ELISA were used to screen 591 randomly selected bulk-milk samples. To clarify discrepancies thirty-nine herds were included in a follow-up study. A second bulk-milk sample and serum samples from 10 young cattle of 6 to 28 month of age per herd were analysed for antibodies against BVDV. The results of this second testing and the detection of viremic animals in 4 herds confirmed the results from initial bulk-milk testing with both tests. The analysed test is suitable for bulk-milk testing although its application is limited by vaccination.

A total of 5204 bulk milk samples were tested for antibodies against bovine viral diarrhea virus (BVDV) classified according to the scheme after Alenius. Forty-five percent of the samples from 2002 were classified as class 0 and class 1, 55% as class 2 and 3. 6420 bulk milk samples from 1997 were classified in an independent study in 65.6% class 0 and 1 and 34.4% in class 2 and 3. In class 0 and class 1 farms only very rarely persistent viremic animals have been found, whereas in class 2 and 3 their presence is highly likely. Our studies with non-selected sera defined the serological screening of bulk milk samples as a promising tool for a possible BVDV eradication program in Bavaria.

We here report on the first case of scrapie in Bavaria. The post mortem of a six year old ewe of the breed German grey Heath with a suspected subclinical calcinosis revealed typical histopathological signs of a spongiform encephalopathy and immunohistochemistry was positive for PrPSc in the cervical part of the spinal cord. Eight out of 18 sheep of the herd showed clinical symptoms.

The genetic variability of the prion protein gene influences the susceptibility to infection with transmissible spongiform encephalopathy (TSE) agents in mice, sheep and possibly mail. Pigs have been shown to be susceptible to the bovine spongiform encephalopathy (BSE) agent after intracerebral, but not after oral inoculation. In these studies, however, only a very limited number of pigs of a restricted genetic background were used. Therefore, the question arose whether those experiments do reflect the susceptibility of the species pig or rather that of a single possibly resistant pig breed. The prion protein gene of a total of 66 pigs from 12 different breeds (2 x Deutsche Landrasse, 3 x Deutsches Edelschwein. 4 x Leicoma, 4 x Duroc, 11 x Pietrain. 6 x Large White, 9 x Hampshire, 2 x Belgische Landrasse, 8 x Schwabisch Hallisches Schwein, 6 x Bunte Bentheimer. 7 x Chinesisches Meishan, 4 x Wildschwein (wild boar)) was amplified by PCR and directly sequenced. All sequences were found to be identical and identical to the published sequence (T. Martin, S. Hughes, K. Hughes, and M. Dawson Biochem. Biophys. Acta 1995; 1270: 211)

Slaughter pigs are the main reservoir for pathogenic Yersinia (Y.) enterocolitica isolates. Particularly meatproducts derived from swine asymptomatically infectedare a potential source of human Yersiniosis. Due to thisfact it is important to have simple, rapid and specificmethods available for the detection of pathogenic Y. enterocolitica in tissue samples from slaughtered pigs.The aim of this study was to validate a 24 h preenrichmentstep in Yersinia-PCR-compatible-enrichment (YPCE) broth followed by a yopT-based PCR-Method forthe rapid detection of pathogenic Y. enterocolitica inorgans and lymphoid tissue of slaughtered pigs. Untilnow, the bacteriological identification of pathogenic Yersinia, described in ISO 10273, is the "goldstandard". To compare the PCR results with the "goldstandard" we choose for the cultural detection a 48hour pre-enrichment step at 25 C in ITC broth followedby plating on CIN agar plates and incubation for 24hours at 30°C. For the validation of the PCR method itwas important to have available samples fromasymptomatically infected pigs. To generate thosesamples Yersinia-free pigs (n = 9) were intragastricallyinfected with a plasmid bearing Y. enterocolitica isolate (DSM 13030). Two additional pigs served asuninoculated controls. Four weeks after infection pigswere slaughtered and 13 samples from each pig weretaken aseptically.In comparison to the conventional cultural examinationthe combination of pre-enrichment in YPCE brothfollowed by yopT-PCR saved about four days ofdiagnostic time. Particularly, in the examined samplesof the palatine tonsil, an organ with the highestcontamination rate in slaughter pigs, demonstrated thePCR method a significantly better sensitivity than thecultural method. In summary, the 24 h pre-enrichmentand subsequent yopT-PCR represents a rapid andsensitiv diagnostic tool for pathogenic Y. enterocolitica in asymptomatically infected pigs at the slaughterhouselevel.

Background Feline Panleukopenia (FPL) is a serious disease of cats that can be prevented by vaccination. Kittens are routinely vaccinated repeatedly during their first months of life. By this time maternally derived antibodies (MDA) can interfere with vaccination and inhibit the development of active immunity. The efficacy of primary vaccination under field conditions was questioned by frequent reports to the Paul-Ehrlich-Institut on outbreaks of FPL in vaccinated breeding catteries. We therefore initiated a field study to investigate the development of immunity in kittens during primary vaccination against FPL. 64 kittens from 16 litters were vaccinated against FPL at the age of 8, 12 and 16 weeks using three commercial polyvalent vaccines. Blood samples were taken before each vaccination and at the age of 20 weeks. Sera were tested for antibodies against Feline Panleukopenia Virus (FPV) by hemagglutination inhibition test and serum neutralisation assay in two independent diagnostic laboratories. Results There was a good correlation between the results obtained in different laboratories and with different methods. Despite triple vaccination 36.7% of the kittens did not seroconvert. Even very low titres of MDA apparently inhibited the development of active immunity. The majority of kittens displayed significant titres of MDA at 8 and 12 weeks of age; in some animals MDA were still detected at 20 weeks of age. Interestingly, the vaccines tested differed significantly in their ability to overcome low levels of maternal immunity. Conclusions In the given situation it is recommended to quantify antibodies against FPV in the serum of the queen or kittens before primary vaccination of kittens. The beginning of primary vaccination should be delayed until MDA titres have declined. Unprotected kittens that have been identified serologically should be revaccinated.