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A disease affecting guinea pigs called 'guinea pig lameness' characterized by clinical signs of depression, lameness of limbs, flaccid paralysis, weight loss and death within a few weeks was first described by Römer in 1911. After a research group in our facility kept laboratory guinea pigs from two different origins together in one room, lameness was observed in two animals. Further investigations revealed a serological immune response against Theiler's murine encephalomyelitis virus (TMEV; GDVII strain) in these animals. Histopathology of the lumbar spinal cord of these animals showed mononuclear cell infiltration and necrotic neurons in the anterior horn. Therefore, all guinea pigs from this contaminated animal unit, from other units in our facility, as well as from different European institutions and breeding centres were screened for antibodies directed against GDVII. Our investigations showed that approximately 80% of all guinea pigs from the contaminated animal unit were seropositive for GDVII, whereas animals from other separate units were completely negative. In addition, 43% of tested sera from the different European institutions and breeding centres contained antibodies against GDVII. The present data confirm that an unknown viral infection causes an immune response in experimental guinea pigs leading to seroconversion against GDVII and that guinea pigs from a commercial breeder are the source of the infection., (© The Author(s) 2015.)

The possibility of modifying the genome in mice has led to an exponential increase in the number of strains that have been developed for biomedical research. This will continue during the next few decades because international programmes plan to develop genetically-modified strains for every known mouse gene. Due to our own experiences and that of colleagues we know that the reproductive performance of many of these modified stains is impeded, despite that the modification is independent from genes that control reproduction. In some cases the spermatogenesis might be disturbed. The reason presumably lies in a defective endocrine function of the testes. This can cause reduced and/or abnormal sperm production. In livestock as well as in humans these disorders can be treated with gonadotropins. One treatment period lasts for the duration of spermatogenesis of the respective species. Up to now, nothing is known about such treatments in laboratory mice to restore or increase reproduction of genetically-modified strains. Spermatogenesis in the mouse lasts approximately 35 days. Therefore, we treated sexually mature male mice of C57BL/6 and BALB/c strains with gonadotropins for this period. The aim of this study was to test the principle suitability of such treatment for the improvement of sperm count, sperm motility, fertilization ability and reproduction.

Individual differences and a rather long-lasting reproductive cycle, as well as the relatively small number of oocytes that mature during one reproductive cycle makes it difficult to establish a cryopreserved stock of preimplantation embryos of the guineapig (Cavia porcellus) when compared with other laboratory rodents. Only a few data for superovulation protocols that can be used for routine laboratory use in guineapigs are available. However, a huge number of different strains exist for many purposes and the establishment of a frozen repository makes sense. Here, we describe the successful freezing of preimplatation embryos of the strain 2BS with a two-step freezing protocol in a freezing medium containing 1,2-propanediol as cryoprotectant. Human menopausal gonodotrophin induced superovulation in the embryo donors.

The Mongolian gerbil serves as an animal model for a wide range of diseases. As these animals are extensively used for the study of Helicobacter pylori-induced gastritis, naturally occurring infections with rodent Helicobacter species in gerbils are a possible source of interference in studies of H. pylori-associated disease. The gerbil stock at the Central Animal Facility in Hannover was persistently infected with H. hepaticus. The aim of this study was to derive Helicobacter species-free Mongolian gerbils. Therefore, germfree gerbil pups were obtained by Caesarean section and the pups were transferred to female rats and mice with recently delivered litters. In total, four Ztm:NMRI mice, four Ztm:SPRD rats and one DA/Ztm rat that originated from a specified pathogen-free area were selected to serve as foster mothers. With this approach, it was possible to obtain Helicobacter-free gerbils. Rearing by mice was more successful than by rats, as six of nine gerbils were reared by mice, but only one of 29 gerbils was reared by rats.

The Mongolian gerbil is an excellent animal model for Helicobacter pylori-induced gastritis in humans. In this study, initially low colonization rates of the H. pylori strains ATCC 43504, SS1, or HP87 inoculated into gerbils caused difficulties in establishing this model. In order to increase the colonization ability and pathogenicity, the clinical HP87 isolate was selected for adaptation to the gerbil stomach by multiple in vivo passages through gerbils. Development of gastritis was examined histologically at 4-52 weeks after infection. The proportion of gerbils which tested positive for H. pylori by culture at four weeks after inoculation gradually increased from 11.1% of gerbils inoculated with HP87 without prior in vivo passage (P0) to 100% of gerbils inoculated with HP87 with seven in vivo passages (P7). In addition, adaptation of HP87 resulted in more severe histopathological changes. Gerbils infected with adapted HP87 (P7) exhibited severe infiltration by monomorphonuclear and polymorphonuclear leukocytes in the mucosa, submucosa, and subserosa of the gastric antrum, as well as epithelial changes consisting of hyperplasia, erosion, and ulceration. Histopathological changes increased in severity from four to 52 weeks after infection. Adaptation of HP87 during its passages through gerbils could be due to genetic changes in bacterial colonization factors. Identification of these changes might be useful to understand the underlying mechanism of gastric adaptation and pathogenesis of H. pylori.