Effect of experimentally induced trichinellosis on the infection with Erysipelothrix rhusiopathiae in rats.

Infection with Erysipelothrix rhusiopathiae in rats infested 20 days earlier with Trichinella spiralis developed more slowly, the clinical and pathoanatomic changes in the joints were expressed to a less extend, and the mortality rate was lower. The erythrocyte sedimentation rate, the precipitin formation and the phagocytic activity of the macrophages did not considerably change. Experiments carried out to elucidate this fact did not reveal any antigenic or antagonistic relationships between parasite and bacterium nor any protective effect of the host's serum. The inhibitory influence of corticosteroids on the defence forces was not completely manifested in the rats infested. This fact might be explained by interrelations depending both on the cycle of helminth development and on the non-specific immunological reactivity of the organism, the latter being stimulated by the helminth invasion.     

A survey of Erysipelothrix insidiosa agglutinating antibody titers in vaccinated porpoises (Tursiops truncatus).

Antibody activity against Erysipelothrix insidiosa was measured in 15 porpoises which had undergone a series of vaccinations, at 6 month intervals, with erysipelas bacterin. Relatively high levels of aggluntinating antibodies were found to persist in the serum for a least 6 months following booster inoculations of the vaccine.     

Ocular lesions in experimental Trypanosoma brucei infection in cats.

Experimental Trypanosoma brucei-infection progressing clinically peak-wise, induces intense proteinleakage in the anterior chamber of cats' and dogs' eyes, with a cyclitislike symptomatology, preceded by hypersensitivity of conjunctiva and respiratory mucosae, together with lacrimation, and facial oedema. The pherogram of aqueous humor is the replica of the serumpherogram at the endstage of the disease and is identical to secondary aqueous. Absence of any significant changes in serumproteins, immunoglobulins and the poor cellular reaction at tissue-level point towards immune unresponsiveness subsequent to experimental protozoal infection. Light-microscopy reveals at the level of the ciliary processes two kinds of cystic formation, the walls of which are formed by ciliary epithelium. One type contains amorphous material next to trypanosomes, macrophages and plasmocyte-like cells; the second type contains also fibrillar structures possibly reminding collagen. Ultramicroscopy suggests these cystic formation to be enlarged ciliary channels. The fenestrated capillary wall showing no changes neither after withdrawal of aqueous, nor after toxic parasite-action, the presence of large proteinmolecules and trypanosomes in the anterior chamber are due to damage to the ciliary epithelium.     

Hepatic lesions in experimental Campylobacter jejuni infection of mice

Mice orally infected with Campylobacter jejuni developed focal infiltrative necrotic lesions in the liver, as determined by both histology and liver function tests. The initial histopathological feature was a focal infiltrative lesion in the parenchyma and portal triads. Foci of infiltrative lesions became necrotic between days 30 and 60 post-inoculation (p.i.). During this period, portal infiltrates increased in severity. From month 4 p.i., focal areas of infiltrative necrosis in the liver parenchyma became extensive. Study of liver function demonstrated mild elevations of transaminases, alkaline phosphatase and lactic dehydrogenase, and also the presence of hypoalbuminaemia. Although histopathological changes of the liver became gradually more marked after day 30 p.i., liver functions of infected mice were most affected at 2 months p.i. The capacity of C. jejuni to induce hepatic lesions seemed to be related to that of organisms to persist in the gall bladder; there was no correlation between biliary carriage in infected mice and positive faecal culture.     

Pulmonary lymphoid lesions in an experimental model of collapsing glomerulopathy in rats

The characterization of lung damage in an experimental model of collapsing glomerulopathy (CG) in rats is described. METHODS: 12 rats were divided into two groups and injected intravenously (iv) with 1 mg/saline in a final volume of 1 ml/ day in the tail vein for 5 days, with fractionated serum from control and CG subjects. Proteinuria was quantified, and the Glomerular filtration rate was calculated based on creatinine clearance (CC). Rats were sacrificed by perfusion fixation at day 5. RESULTS: Rats injected with serum from CG patients developed proteinuria (p<0.001). A decrease in CC (0.68+/-0.19) in these rats was also observed. Glomerular tuft retraction and mesangial proliferation was observed in all rats receiving serum from the CG patients. Peribronchiolar infiltrate integrated mainly by lymphocytes, was identified in all CG rats. In some areas this infiltration disrupted the basement membrane and damaged the epithelium. No histopathological abnormalities in the kidney or lungs were found in rats receiving control serum. CONCLUSION: Patchy pulmonary lymphoid infiltrates were found in the CG model. Up to now there was no information about pulmonary lymphoid infiltration in CG patients. Besides fluid overload due to renal insufficiency or a nephrotic syndrome, other causes of pulmonary involvement in CG patients should be explored.     

Carrageenin-induced experimental pneumonia in rats.

The authors verified the possibility of modelling pneumonia by the intratracheal administration of carrageenin solution into the lungs of rats. The most satisfactory dose was found to be 0.5 ml 0.7% carrageenin solution administered at 40 degrees C. The disease, evaluated by the morphological and functional signs, culminated after two days. Both macroscopically and histologically the lungs displayed typical signs of catarrhal suppurative aspiration bronchopneumonia. Functionally, marked tachypnoea (mean 180 cycles/min as against 110 c/min in the conscious controls) and raised functional residual capacity were found. A drop in the respiration rate and in FRC after bilateral cervical vagotomy indicated that a reflex component participates in the origin of the above two signs.     

Wild boars: A potential source of Erysipelothrix rhusiopathiae infection in Japan

The potential role of wild boars as a source of erysipelas infection was investigated. An ELISA test of wild boar serum samples from 41 prefectures in Japan revealed that proportions of the Erysipelothrix rhusiopathiae‐positive samples were very high in all the prefectures, and the mean positive rate was 95.6% (1312/1372). Serovars of E. rhusiopathiae isolates from wild boars were similar to those of previously reported swine isolates, and all serovar isolates tested were found to be pathogenic to mice. These results suggest that wild boars in Japan constitute a reservoir of E. rhusiopathiae and may pose risks to other animals.     

Persistence of Staphylococcus aureus L-form during experimental lung infection in rats

The course of pulmonary infection in rats infected by intranasal inoculation with a Staphylococcus aureus stable protoplast L-form was studied. Blood and bronchoalveolar samples were taken on days 3, 7, 14 and 30 after challenge and were investigated by microbiological, electron-microscopic, cytochemical and cytometric methods. The electron microscopic data and isolation of L-form cultures from bronchoalveolar samples at all experimental times demonstrated the ability of S. aureus L-form cells to internalize, replicate and persist in the lungs of infected rats to the end of the observation period, in contrast to the S. aureus parental form. It was found that persisting L-form evoked ineffectual phagocytose by alveolar macrophages and low but long-lasting inflammatory reaction in rats. The experimental model of pulmonary infection with S. aureus L-form suggests that the cell-wall-deficient bacterial forms may be involved in the pathogenesis of chronic and latent lung infections.