Incidence, epizootiology and control of viral haemorrhagic disease of rabbits and the European brown hare syndrome in Germany.

Viral haemorrhagic disease (VHD) among domestic and wild rabbits and European brown hares have been observed in most of the Federal states of Germany. Acute outbreaks of viral haemorrhagic disease are most prevalent in small, fancy domestic rabbitries, with mortality varying between 5 and 90%, while mostly sporadic losses due to VHD are seen among wild rabbits. In hares, accumulated losses from the European brown hare syndrome (EBHS) can occasionally be observed in areas where fresh green feed, such as young O.O-rape plants, is available. VHD of rabbits and EBHS are caused by calicivirus strains. The natural virus reservoirs are wild rabbit and hare populations. Mutual infection of rabbits and hares seems to be possible. Transmission and spread of infectious virus occurs by direct contact of animals, or indirectly by contaminated excrement, green feed or living vectors. Calicivirus infections are widespread in several states, with accumulation of losses among domestic and wild rabbits by VHD, or in hares by EBHS, within certain areas. Disease hygiene, together with vaccination, are the officially preferred control measures in domestic rabbitries.

[Infectious factor diseases in domestic small animals (carnivorous and herbivorous fur animals, wool and meat rabbits]. / Infektiöse Faktorenkrankheiten bei Nutzkleintieren (karnivore und herbivore Pelztiere, Woll- und Fleischkaninchen).

Infectious factorial diseases of domesticated small animals are infection dependent diseases, whose pathogenesis is finally activated by additional, secondary factors, that influence the multiplying and spreading of latent and clinical symptomless infective agents present in the animals. These factorial diseases are not autonomous infectious processes, but only special types and courses of diseases by secondary activated infective agents. Secondary factors may be of exogenous origin (housing, climate, feeding, managing) or may arise by endogenic processes (immunity, resistance disregulations a.o.). In fur bearing animals and rabbits infectious factorial diseases arise by activation of latent, symptomless infections of mucosal membranes in the nose and oral cavity, in the intestinal tract, in the descending urinary tract and on the external skin. The majority of infection activating secondary factors go back on wrong housing conditions, extreme climate, malnutrition and simultaneous infections, but also animal specific situations and immunosuppression may influence the activation of latent infections. - Typical factorial diseases in fur bearing animals and rabbits are: the infectious coryza (Pasteurella multocida, Bordetella bronchiseptica) in rabbits, the Coli-dysentery and the enterotoxemia in rabbits and herbivorous fur animals, the ascending infections of urinary tract, particular in young male minks, and the different types of microbial dermatitis in all small animals. - In the prevention and control of infectious factorial diseases the improvement of housing and living conditions as well as feeding the animals with species conforming and nonobjectionable food are most important and essential measures.

Oligoribonucleotide map and protein of CMII: detection of conserved and nonconserved genetic elements in avian acute leukemia viruses CMII, MC29, and MH2.

RNA and protein of the defective avian acute leukemia virus CMII, which causes myelocytomas in chickens, and of CMII-associated helper virus (CMIIAV) were investigated. The RNA of CMII measured 6 kilobases (kb) and that of CMIIAV measured 8.5 kb. By comparing more than 20 mapped oligonucleotides of CMII RNA with mapped and nonmapped oligonucleotides of acute leukemia viruses MC29 and MH2 and with mapped oligonucleotides of CMIIAV and other nondefective avian tumor viruses, three segments were distinguished in the oligonucleotide map of CMII RNA: (i) a 5' group-specific segment of 1.5 kb which was conserved among CMII, MC29, and MH2 and also homologous with gag-related oligonucleotides of CMIIAV and other helper viruses (hence, group specific); (ii) an internal segment of 2 kb which was conserved specifically among CMII, MC29, and MH2 and whose presence in CMII lends new support to the view that this class of genetic elements is essential for oncogenicity, because it was absent from an otherwise isogenic, nontransforming helper, CMIIAV; and (iii) a 3' group-specific segment of 2.5 kb which shared 13 of 14 oligonucleotides with CMIIAV and included env oligonucleotides of other nondefective viruses of the avian tumor virus group (hence, group specific). This segment and analogous map segments of MC29 and MH2 were not conserved at the level of shared oligonucleotides. CMII-transformed cells contained a nonstructural, gag gene-related protein of 90,000 daltons, distinguished by its size from 110,000-daltom MC29 and 100,000-dalton MH2 counterparts. The gag relatedness and similarity to the 110,000-dalton MC29 counterpart indicated that the 90,000-dalton CMII protein is translated from the 5' and internal segments of CMII RNA. The existence of conserved 5' and internal RNA segments and conserved nonstructural protein products in CMII, MC29, and MH2 indicates that these viruses belong to a related group, termed here the MC29 group. Viruses of the MC29 group differ from one another mainly in their 3' RNA segments and in minor variations of their conserved RNA segments as well as by strain-specific size markers of their gag-related proteins. Because (i) the conserved 5' gag-related and internal RNA segments and their gag-related, nonvirion protein products correlate with the conserved oncogenic spectra of the MC29 group of viruses and because (ii) the internal RNA sequences and nonvirion proteins are not found in nondefective viruses, we propose that the conserved RNA and protein elements are necessary for oncogenicity and probably are the onc gene products of the MC29 group of viruses.

[Investigations into the relationship of cell susceptibility and antibody formation and its importance in the pathogenesis of avian leukosis]. / Untersuchungen uber die Beziehungen Zwischen der Zellempfanglichkeit und Antikorperbildung und ihre Bedeutung in der Pathogenese Aviarer Leukosen.

Crossbred progeny from matings of Leghorn males (lines M and G), predominantly susceptible to leukosis infection, and females from a predominantly leukosis-resistant line (line R) showed a high incidence of mortality from spontaneous leukosis. Immunological tests revealed that this field infection was caused by a subgroup A leukosis virus. Tests for susceptibility to infection and presence of RSV antibodies in embryos and pullets respectively of lines R, G and M yielded the following results: line R appears to be predominantly resistant to BH-RSV (RAV1) and BH-RSV (RAV2) (subgroups A and B), line G predominantly resistant to BH-RSV (RAV2) (subgroup B), but susceptible to BH-RSV (RAV1 ) (subgroup A), while line M is predominantly susceptible to both BH-RSV (RAV1 ) and BH-RSV (RAV2) (subgroups A and B). Resistance to infection and formation of antibodies are closely interrelated. Resistant chickens are generally free of antibodies specific to antigens of the particular subgroup. Hens resistant to infections from a certain subgroup of leukosis viruses are unable to produce antibodies against this antigen and therefore cannot protect their progeny by giving them sufficient maternal antibody. Matings of such resistant hens with males homozygous dominant susceptible to leukosis infections will produce progeny which are not only susceptible to leukosis infections but which also lack maternal antibodies to protect them against leukosis viruses during the particularly critical first few days of life.