The diagnosis and treatment of acid-base deranged dogs infected with Babesia canis.

A study was made of the acid-base status of Babesia canis infected dogs judged unlikely to recover after specific babesicidal drug therapy despite the use of blood transfusion and other conventional supportive measures. Such cases were invariably acidotic and responded well and often dramatically to supportive intravenous sodium bicarbonate administration. Elevated blood urea nitrogen, also responded gratifyingly to this procedure. The rationale is discussed in some detail.

[Studies on the nephrotoxicity of cephaloridine in the mouse (author's transl)]. / Nephrotoxizitätsstudien mit Cephaloridin an der Maus.

The nephrotoxicity of 1-[2-carboxy-8-oxo-7-(2-thienylacetamido)-5-thio-1-azabicyclo[4.2.0]oct-2-en-3- yl]methyl-pyridinium hydroxide (cephaloridine, Glaxoridin) in mice was investigated histopathologically in a series of 14 experiments. Using the PAS-reaction lesion formation consisting of epithelial desquamation in the tubuli contorti proximales, coarse cytoplasmic granulation of the tubuli recti proximales epithelium and hyaline cast formation was detected. Regeneration of the tubular epithelium followed subsequently. Optimal lesion formation was detected when mice were given two s.c. injections of an aqueous solution of the compound and the post mortem was carried out two days later. B5D2F1 hybrid mice were more sensitive than NMRI mice. However, a preexperimental acclimatisation period of at least ten days was necessary to obtain reproducible results.

[Nephrotoxicity of gentamicin in mice]. / Nephrotoxizitätsstudien mit Gentamicin an der Maus.

Gentamicin sulfate was tested for nephrotoxicity in B6D2F1 hybrid mice after s.c. and i.p. administration. By a series of experiments designed to study histological lesions (tubular epithelial desquamation, intracytoplasmatic coarse granulation of epithelial cells) the following procedure showed favourable results: withdrawal of drinking water 24 h before start of experiment--one daily s.c. administration during four days--post mortem examination after further 24 h. Within the epithelium of the proximal tubules two distinct lesions can be distinguished morphologically 1. an acute necrosis giving rise to acute cytolysis, 2. at a lower segment of the nephron, intracytoplasmatic storage of PAS-positive granules in cells, which are devoid of a brush border but have otherwise experienced only slight alterations. The morphology of these lesions is similar to that after administration of toxic doses of cephaloridine though the resorption of the compounds takes place in the case of gentamicin at the free cell border whereas after cephaloridine administration the compound enters the tubular epithelial cells via the basal membrane.

Studies of lung infections caused by Pseudomonas aeruginosa in mice treated with cyclophosphamide.

An experimental Pseudomonas aeruginosa lung infection was induced by aerosol exposure in mice which had been pretreated with cyclophosphamide. A single dose of 200 mg/kg cyclophosphamide resulted in leukopenia which lasted for three days. At the lowest PMN levels, the mice were exposed to aerosols containing varying doses of bacteria. The survival time of the mice and the number of viable bacteria in their lungs were determined. A dramatic rise in the viable counts of Pseudomonas organisms was found between 18 and 24 hours after infection. Mice which had not been pretreated with cyclophosphamide remained healthy and did not show any lung lesions. The number and phagocytic function of the alveolar macrophages remained unaltered after cyclophosphamide treatment. Thus, PMNs seem to play an important role in the lung's early defence mechanisms against Pseudomonas aeruginosa. This animal model could be of use in evaluating additional therapies for lung infections caused by Pseudomonas aeruginosa.

[Clinical and histopathological findings in mycoplasmal polyarthritis of rats. I. Course of infection during the first 8 days (author's transl)]. / Klinische und histopathologische Befunde bei der Mykoplasma-Polyarthritis der Ratte. I. Der Ablauf der Infektion in den ersten 8 Tagen

Polyarthritis in rats could be induced by intraperitoneal infection with M. arthritidis. The mycoplasma culture alone or in combination with infusorial earth was used as inoculum. The histopathological changes consisted of initial lesions in the transitional zone of the articular capsule which could be attributed to disturbances of vascular permeability. After two days suppurative arthritis occurred, which was accompanied by massive inflammatory lesions of the articular capsule and of the periarticular tissues. Towards the end of the observation period erosions of cartilage, pannus formation and periarticular foci of purulent necrobiosis were found. Especially the synovial membrane was subjected to profound changes and dense cellular infiltration. The cell infiltration, mesenchymal proliferation and changes of vascular permeability showed variations in timing and degree depending on the modi of infection. The histological examinations of organs indicated generalization of the infection.

[Clinical and histopathological findings in mycoplasmal polyarthritis of rats. III. Course of infection during the weeks 7-30 and 54-61 (author's transl)]. / Klinische und histopathologische Befunde bei der Mykoplasma-Polyarthritis der Ratte. III. Der Krankheitsablauf in der 7.-30. und 54.-61. Woche

Clinical, microbiological and histological findings of the late phase of experimentally induced Mycoplasma-polyarthritis in rats are described. Investigations were carried out between the 7.-30. week and between the 54-61. week p.i. M. arthritidis could be reisolated from affected joints regularly up to the 7th week p.i. Thereafter until 12th week only occasional recovery was possible. The healing process of affected joints dominated signs of arthritis which could be confirmed histologically as a purulent process. The alterations of carpal and tarsal joints were divided into purulent, chronic deforming and chronic minor lesions. The findings derived from investigation of joints and parenchymatous organs during the course of the disease are discussed.

Bronchoalveolar lavage in dogs; analysis of proteins and respiratory cells.

In an attempt to establish the normal values, bronchial alveolar lavage (BAL) of portions of the right upper lobe was done during fiberoptic bronchoscopy in 18 Beagle dogs of various ages. Albumin, IgA and IgG were identified in BAL fluids. The respiratory cells obtained were, in the order of decreasing occurrences, alveolar macrophages, lymphocytes, epithelial cells and neutrophils. No age-related changes were found in the content of immunoglobulins or in the differential cell counts of respiratory cells. Bacterial cultures of BAL were invariably contaminated with resident flora of the upper respiratory tract. Therefore, in determining the etiology of pulmonary infections, the results of such cultures should be interpreted with caution. As an aid to diagnosis of pulmonary diseases in dogs, the analysis of BAL fluid components could be helpful when compared with findings in healthy animals.

Growth of some attenuated influenza viruses in hamster tracheal organ cultures.

Hamster tracheal organ cultures were infected with different influenza viruses and the metabolic activity measured using a tetrazolium reduction assay. In addition, relative ciliary activity was observed, virus multiplication measured, and histological studies were made. The hamster organ cultures proved relatively simple to set up and were sensitive to infection with influenza viruses; and the tetrazolium reduction was a reliable objective measure of relative tissue damage correlating well with histological and virological findings as well as with visual assessment of ciliary activities.

[Systemic reactions in rats following the initiation of a local inflammatory process by subcutaneous administration of spirits of turpentine]. / Systemische Reaktionen in Ratten nach Setzung lokal entzündlicher Prozesse durch subcutane Terpentinöl-Gaben.

Local inflammation was induced in rats by single (1 x 4 ml/kg) or multiple (14 X 0.2 ml/animal) infections of turpentine. The induction of inflammatory processes in both groups resulted in anemia and granulocytosis following an initial leukopenia. Thrombopenia on the second day, followed by thrombocytosis, was also observed in both groups. Studies on blood chemistry parameters revealed a decline in serum albumin; elevation of alkaline phosphatase in serum was observed only after multiple injection of turpentine. In these animals an elevation in the weights of spleen and adrenals and a reduction in the weight of thymus were also found.

Protection of mice against lethal endotoxemia by lipid X is mediated through inhibition of neutrophil function.

The effects of lipid X and 3-aza-lipid X on in vitro neutrophil function were related to their ability to inhibit the toxicity of endotoxin in galactosamine-sensitized mice. In vitro, lipid X and 3-aza-lipid X (100 ng/ml) blocked completely endotoxin (100 ng/ml)-enhanced neutrophil aggregation, superoxide anion generation, and release of beta-glucuronidase in response to a chemotactic tripeptide, f-met-leu-phe (10(-7) M). In vivo, lipid X at 250 micrograms/mouse (but not 3-aza-lipid X at a similar dose) protected groups of 10 mice from an otherwise lethal dose of endotoxin in galactosamine-sensitized mice when it was administered IV 4 hr or 2 hr before endotoxin challenge. The minimum effective dose of lipid X that could protect 50% of the challenged mice was calculated to be 715 micrograms/kg. However, lipid X failed to suppress neutrophil infiltration into the lungs. The ability of lipid X to inhibit endotoxin-induced neutrophil responses and to protect against lethal endotoxemia may be due to induction of early phase tolerance to endotoxin by the compound.