Clindamycin-induced enterocolitis in hamsters as a model of pseudomembranous colitis in patients

Stools from a patient with antibiotic-associated colitis and cecal contents from a hamster with clindamycin-induced enterocolitis were compared in a cytotoxicity assay to determine common properties. Both specimens produced actinomorphic changes in human amnion cells at 10(-7) dilutions. The toxin was acid labile, heat labile, nonether extractable, non-dialyzable, and produced maximum activity at 60% with ammonium sulfate precipitation. Cytotoxicity was neutralized with clostridial antitoxin but not with equine serum. Clostridium difficile was recovered in high concentrations in specimens from both the hamster and patients. The supernatants of these C. difficile strains produced cytoxic effects which were also neutralized by clostridial antitoxins. These results indicate that clindamycin-induced enterocolitis in hamsters is a model of human disease and implicate toxin-producing clostridia as responsible agents.     

Experimental biological model of bacillary dysentery

Summary Experiments were carried out aimed to reproduce the experimental model of Flexner's dysentery in kittens.All the kittens infected with the typical Flexner's strain showed after the incubation period (5 to 6 days) clinical symptoms similar to that of the dysentery in man.Clinical and laboratory observations on the infected animals make it possible to assume that the kittens may serve as a model for studying problems of pathogenesis and immunity in bacillary dysentery.Presented by L. A. Zilber, active Member of the Academy of Medical Sciences, USSR     

Canine X-linked muscular dystrophy as an animal model of Duchenne muscular dystrophy: a review.

Canine X-linked muscular dystrophy is a spontaneously occurring, progressive, degenerative myopathy of dogs that is clinically and pathologically similar to Duchenne muscular dystrophy in man. The molecular basis for the disease has been shown to be a lack of dystrophin, the protein product of the Duchenne muscular dystrophy gene. Breeding colonies of dystrophic dogs have been established. This report reviews the findings of genetic, clinical, pathologic, molecular biologic, and immunocytochemical studies of the canine model, and compares the features of the canine disease to those of Duchenne dystrophy in man.     

Experimental cryptosporidiosis in hamsters.

A new laboratory animal model for experimental cryptosporidiosis is described. Adult immunosuppressed hamsters were infected per os with 0.5 x 10(5) and 1 x 10(5) Cryptosporidium oocysts of calf origin. The mean numbers of oocysts shed per gram of feces per day and the patterns of infection are described. The susceptibility to Cryptosporidium infection, the total number of oocysts shed (a thousand times the infective dose), and the ease of handling in laboratory conditions make hamsters a good animal model for cryptosporidiosis.     

Experimental sporotrichosis in Syrian hamsters.

Syrian hamsters were infected with Sporothrix schenckii by subcutaneous footpad inoculation. Two types of infection could be uniformly induced: a self-limited, lymphatic infection resembling the classical disease in humans, and a generalized nonfatal infection. An infecting dose of approximately 5,300 yeast cells produced the localized subcutaneous-lymphatic disease which was limited to a single limb. In contrast, a 1,000-fold increase in the inoculum temporarily overwhelmed the animals' defense mechanisms, producing a systemic infection involving the liver and spleen. These models were used to demonstrate the development of increased resistance to subsequent infection following either infection or active immunization with ribosomal fractions or trypsinized cell wall antigens of S. schenckii incorporated in Freund complete adjuvant. Agglutination titers were detectable in all animals that were either infected or immunized. In one group of infected animals, the titers persisted for at least 1 year after three booster doses of Formalin-killed S. schenckii. The ability to produce an infection in hamsters which closely resembles the disease seen in humans makes the animal a good model with which to study experimental sporotrichosis.     

A new experimental model of cecal amebiasis in rats

The young rat was used as an experimental model of caecal amebiasis by implanting, without injury of the caecum, a suspension of E. histolytica trophozoites gnotoxenic strain Rahman of high virulence. The degree of pathogenicity is demonstrated by the macroscopic aspect of caecum, by the density of trophozoites and by an anatomopathologic examination. As a correlation exits between all these macroscopic parameters and histology, a degree of illness is fixed which include several macro- and microscopic criteria. This model enables to observe the different phases of cicatrization and of recovering of young rats and so to appreciate the activity of antiamebic agents.     

Canine X-linked muscular dystrophy as an animal model of Duchenne muscular dystrophy: A review

Canine X-linked muscular dystrophy is a spontaneously occurring, progressive, degenerative myopathy of dogs that is clinically and pathologically similar to Duchenne muscular dystrophy in man. The molecular basis for the disease has been shown to be a lack of dystrophin, the protein product of the Duchenne muscular dystrophy gene. Breeding colonies of dystrophic dogs have been established. This report reviews the findings of genetic, clinical, pathologic, molecular biologic, and immunocytochemical studies of the canine model, and compares the features of the canine disease to those of Duchenne dystrophy in man.     

Hereditary muscular dystrophy in mdx mice as a homologous model for introduction of cell technologies in the treatment of progressive muscular dystrophies in humans

Life-time monitoring of the main clinical and laboratory manifestations of hereditary muscular dystrophy in mdx mice confirmed the presence of mutation in exon 23 of dystrophin gene and the absence of this protein in skeletal muscles of mutant animals. Muscular dystrophy in mice was similar to human progressive muscle disorder, which allows the use of this model for the development of cell technologies for the treatment of hereditary muscular diseases in humans.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 10, pp. 477–480, October, 2004     

Hereditary muscular dystrophy in MDX mice as a homologous model for introduction of cell technologies in the treatment of progressive muscular dystrophies in humans

Life-time monitoring of the main clinical and laboratory manifestations of hereditary muscular dystrophy in mdx mice confirmed the presence of mutation in exon 23 of dystrophin gene and the absence of this protein in skeletal muscles of mutant animals. Muscular dystrophy in mice was similar to human progressive muscle disorder, which allows the use of this model for the development of cell technologies for the treatment of hereditary muscular diseases in humans.Translated from Byulleten Eksperimentalnoi Biologii i Meditsiny, Vol. 138, No. 10, pp. 477–480, October, 2004     

Myopathy phenotype in transgenic mice expressing mutated PABPN1 as a model of oculopharyngeal muscular dystrophy

Autosomal dominant oculopharyngeal muscular dystrophy (OPMD)is a late-onset disorder characterized clinically by progressiveptosis, dysphagia and limb weakness, and by unique intranuclearinclusions in the skeletal muscle fibers. The disease is causedby the expansion of a 10-alanine stretch to 12–17 alanineresidues in the poly(A)-binding protein, nuclear 1 (PABPN1;PABP2). While PABPN1 is a major component of the inclusionsin OPMD, the exact cause of the disease is unknown. To elucidatethe molecular mechanism and to construct a useful model fortherapeutic trials, we have generated transgenic mice expressingthe hPABPN1. Transgenic mice lines expressing a normal hPABPN1with 10-alanine stretch did not reveal myopathic changes, whereaslines expressing high levels of expanded hPABPN1 with a 13-alaninestretch showed an apparent myopathy phenotype, especially inold age. Pathological studies in the latter mice disclosed intranuclearinclusions consisting of aggregated mutant hPABPN1 product.Furthermore, some TUNEL positive nuclei were shown around degeneratingfibers and a cluster of it in the lesion in necrotic musclefibers. Interestingly, the degree of myopathic changes was moreprominent in the eyelid and pharyngeal muscles. Further, muscleweakness in the limbs was apparent as shown by the fatigabilitytest. Nuclear inclusions seemed to develop gradually with aging,at least after 1 week of age, in model mouse muscles. We establishedthe first transgenic mouse model of OPMD by expressing mutatedPABPN1, and our model mice appear to have more dramatic alternationsin myofiber viability. ^* To whom correspondence should be addressed. Tel: +81 963736083; Fax: +81 963736599; Email: yamamura{at}gpo.kumamoto-u.ac.jp     

The feasibility of using Chinese hamsters as an animal model for aneuploidy

The utility of Chinese hamsters as a test species for aneuploidy analysis was studied using four chemicals--vincristine, methyl 2-benzimidazole carbamate (MBC), nocodazole, and cyclophosphamide. Ten or more male Chinese hamsters were used per dose and bone marrow was removed at intervals of 6-96 hr. Slides were coded and 50-100 metaphases were analyzed per animal. A metaphase with more than 22 chromosomes was classified as a hyperploid cell, and the data were evaluated by using a one-tailed Fisher's exact test. In experiments using vincristine, MBC, and nocodazole, the frequencies of hyperploid cells were 0.43, 1.14, and 0.91%, respectively, for the control groups. In the experiment using cyclophosphamide, the control value frequency was 3.75%. The treated groups showed no significant increase in hyperploid frequencies when compared to concurrent controls at each of the treated times, except the value at 24 hr for the group that had been treated with vincristine at 0.75 mg/kg. However, this increase was not significant when compared to the overall value for pooled controls, with or without the cyclophosphamide control. Therefore, no significant effects due to chemical treatment were obtained in the present study. The results illustrate the extent of animal-to-animal as well as experiment-to-experiment variability in hyperploid frequencies and the importance of incorporating concurrent controls in assays for aneuploidy.