Helicobacter pylori-induced gastritis in experimentally infected conventional piglets.

A conventional nonmutant animal that could be experimentally infected with Helicobacter pylori isolates would be a useful animal model for human H. pylori-associated gastritis. Gnotobiotic and barrier-born pigs are susceptible to H. pylori infection, but attempts to infect conventional pigs with this bacterium have been unsuccessful. In the present study, a litter of eight 20-day-old crossbreed piglets were purchased from a commercial farm. Six of them were orally challenged two to five times at different ages, between 29 and 49 days, with doses of H. pylori inoculum containing approximately 10(9) bacterial cells. Two animals served as controls. The inoculation program began 2 days postweaning when the piglets were 29 days of age. Prior to every inoculation, the piglets were fasted and pretreated with cimetidine, and prior to the first and second inoculation each piglet also was pretreated with dexamethasone. The challenged piglets were euthanasized between 36 and 76 days of age. H. pylori colonized all six inoculated piglets. The pathology of the experimentally induced gastritis was examined macroscopically and by light and electron microscopy. H. pylori induced a severe lymphocytic gastritis in the conventional piglets and reproduced the large majority of the pathologic features of the human disease. Therefore, the conventional piglet represents a promising new model for study of the various pathogenic mechanisms involved in the development of lesions of the human H. pylori-associated gastritis.

Masticatory and skeletal muscle myositis in canine leishmaniasis (Leishmania infantum).

Twenty-four dogs with a parasitologically and serologically established diagnosis of leishmaniasis were studied to investigate the atrophy of the masticatory muscles which commonly occurs in this disease, and to compare the lesions in the masticatory muscles with those in the cranial tibial muscles. The 24 animals were divided into three groups of eight, group A dogs with no muscular atrophy, group B dogs with different degrees of atrophy in the masticatory and skeletal muscles, and group C dogs with similar degrees of atrophy in the masticatory and skeletal muscles. Increased activities of creatine phosphokinase and lactate dehydrogenase were recorded in only some of the dogs in groups B and C, but there were no significant differences between the mean activities in the three groups. Electromyographic changes indicating myopathy and involving both the temporalis and cranial tibial muscles, were observed in two of the dogs in group A, seven of those in group B, and in all the dogs in group C. Muscle histopathology revealed a variable degree of muscle fibre necrosis and atrophy, mononuclear infiltrates and neutrophilic vasculitis in all the dogs except two in group A. Leishmanial amastigotes were found within macrophages and myofibres in 16 of the dogs, some in each group. IgG immune complexes were detected in muscle samples, and circulating antibodies against myofibres were detected in serum samples from all the 24 dogs.

Ultrastructure of Sarcocystis tenella (Sarcocystis ovicanis).

The ultrastructure of the parasitophorous cyst, the metrocytes and merozoites of Sarcocystis tenella (S. ovicanis) was studied. The general ultrastructural features of the cyst wall and the cells of the protozoan, previously described by other authors, were confirmed. The vesicle-like invaginations of the unit membrane (primary wall) of the cyst are identical with the micropinocytic pits of other animal cells, and we believe that they contribute to the nutritional process of the cyst. The Golgi apparatus must be related to the granular endoplasmic reticulum, since the first cisterna of the curved side of the stack appeared to originate from it. The structure of the micropore was similar to that previously described by other workers, the only difference being that in this study, material was frequently observed inside the lumen. This observation led us to support the previously suggested nutritive role. In addition, crystalloid material limited by cytoplasmic membrane was often observed, but the manner of its formation and role remain unknown.

[Changes in the myocardium in encephalomyocarditis of pigs]. / Veränderungen des Myokards bei Schweineenzephalomyokarditis.

The myocardial lesions of pigs (age from 2.5 to 3.5 month) with encephalomyocarditis virus infection are presented. The disease is caused by members of the genus Cardiovirus (family Picornaviridae). In Greece it was first observed 1987 in two stables of pig-breeders with a mortality of 80%. The macroscopic changes are characterized by a myocardial degeneration with greyish pale linear or round foci and by an accumulation of a clear red to yellow fluid in the pericardium and the pleural cavity. The most important histologic changes of the hearts are a diffuse or focal myocarditis with a severe infiltration of histiocytes, lymphocytes and plasma cells. Furthermore, degeneration and necrosis of cardiac muscle cells are observed. Electron microscopic investigations of the myocardial cells reveal mild mitochondrial edema, severe perinuclear and intranuclear edema, myelin figures, intra cisternal sequestrations of the rough endoplasmic reticulum, disorganization of the myofibrillar Z-line, and crystalloid viral structures between the mitochondria. Polyribosomes and accumulations of viral particles are frequently found in membrane bound cysts within myocardial cells and the capillaries. Furthermore, viral particles (single or in cysts) and crystalloid viral structures are observed in the cytoplasm of edematous endothelial cells.