[Epidemiologic characteristics of hemorrhagic fever with a renal syndrome in central Povolzh'e].
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Effects of either sterigmatocystin or aflatoxin, alone or in combination, given orally to guinea pigs were studied. Sterigmatocystin and aflatoxin B1 given alone and in combination at 4.2 mg/day and 0.01 mg/day, respectively, markedly reduced body weight. Although changes in total serum protein were not marked in any of the guinea pigs in this study, sterigmatocystin given alone and aflatoxin given alone significantly ( less than 0.05) decreased alpha2-globulin. The combination of toxins significantly (P less than 0.01) increased albumin and significantly (P less than 0.01) decreased both alpha2- and beta-globulins. Sterigmatocystin depressed complement activity, although not significantly. However, the combination of sterimatocystin with 0.01 mg of aflatoxin B1/day (an amount that does not affect complement activity alone) significantly (P less than 0.01) reduced complement activity. Increased severity of lesions was not found in guinea pigs given aflatoxin at 0.01 mg of B1 equivalents/day in addition to the sterigmatocystin.
A naturally occurring, chronic disease of the respiratory tract was investigated from the time of its onset to completion of life-time studies in a colony of rats. The disease was characterized by peribronchial lymphoid cuffing, suppurative bronchitis, bronchiectasis and bronchial abscesses. Its onset in the colony occurred a few months after an epizootic of Sendai virus infection. Limited retrospective serological testing indicated that Mycoplasma pulmonis may have been present in the colony at that time and continued to persist throughout life in some rats in the colony. Although of uncertain significance, light and electron microscopy consistently demonstrated many filamentous bacteria between the cilia on respiratory epithelium and free in bronchial exudate in these cases. Attempts to culture this organism on artificial media were unsuccessful.
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Fourteen monogenic cutaneous disorders of man are compared to similar gene defects in animals. The traits are classified into two groups. In the first group, an identity (homology) of the underlying gene defects is likely. This group includes oculo-cutaneous albinism, Chédiak-Higashi syndrome, aplasia cutis congenita, Ehlers-Danlos syndrome (type I), hypohidrotic ectodermal dysplasia of the Christ-Siemens-Touraine type, X-linked dominant chondrodysplasia punctata, ichthyosis congenita gravis, Menkes syndrome, erythropoetic porphyria, porphyria cutanea tarda, and acrodermatitis enteropathica. In the second group, the traits are similar but the question of their homology cannot be settled. It includes alopecia congenita, hidrotic ectodermal dysplasia of the Clouston type, and hereditary lymphedema. The existence of identical mutations in man and animals provides evidence for the close relationship between the various mammalian species. Homologous traits affecting the skin are of practical importance since the use of these animal models may help to answer those questions which cannot be answered by performing research in human patients.
Premature activation of proteolytic zymogens (trypsinogen, chymotrypsinogen) as an early step in the pathogenesis of exocrine pancreatic insufficency (EPI) syndrome in CBA/J mice was investigated in electrophoresed pancreatic homogenates. Polyacrylamide gels containing extracts from control pancreas required prior activation of trypsinogen and chymotrypsinogen (with exogenously added enterokinase and trypsin, respectively) to produce activity staining with specific synthetic substrates. On the contrary, bands of activity staining in gels containing homogenates from mice with EPI syndrome could be readily detected without trypsin or enterokinase preincubation. Subcellular fractionation of control and diseased pancreas revealed that the premature intracellular proteolysis was confined to the zymogren granule fraction, which, even in very moderately affected pancreases (10 to 30% acinar cell autolysis), was very labile in vitro. These proteolytic events reflect the biochemical consequences of zymogen granule destabilization that were observed at the ultrastructural level.
Preputial gland abscesses were found in 321 (1.8%) of 17,422 mice from our production colonies. The lesions were observed only in males, and Staphylococcus aureus was isolated in pure culture from 84% of the cases. Experimental transmission of the disease was successfully accomplished through injection of Staphylococcus aureus into the penile urethra.
Feline and canine cardiomyopathies (primary myocardial diseases) were reviewed and divided into three groups based on the clinical, hemodynamic, angiocardiographic, and pathologic findings: (1) feline and canine hypertrophic cardiomyopathy, (2) feline and canine congestive (dilated) cardiomyopathy, and (3) feline restrictive cardiomyopathy. All three groups consisted predominantly of mature adult male cats and dogs. Cardiomyopathy in the hamster and turkey was also reviewed. The most common presenting signs were dyspnea and/or thromboembolism in the cat, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (groups 1 and 3) or without (group 2) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end-diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (group 1), left ventricular dilatation (group 2), or midventricular stenosis (group 3). Some cats in groups 1 and 3 also had evidence of left ventricular outflow obstruction. The principal pathologic findings in all of the cats and dogs were left atrial dilation, hypertrophy, increased septal:left ventricular free wall thickness ratio with disorganization of cardiac muscle cells (group 1); dilatation of the four chambers with degeneration of cardiac muscle cells (group 2); and extensive endocardial fibrosis and adhesion of the left ventricle (group 3). Aortic thromboembolism was commonly observed in the cats of all three groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat or dog is similar to the three forms of cardiomyopathy in humans (hypertrophic, congestive, and restrictive).
Seeds of horse chestnut (Aesculus hippocastanum), Ohio buckeye (A glabra), and yellow buckeye (A octandra) were tested for toxicity to 2-week-old Leghorn chicks and adult female Syrian hamsters. The LD50 of the water soluble portion of alcoholic extracts of horse-chestnut seeds (for hamsters and chicks) and of dried, powdered seeds (chicks only) was determined. The LD50 for a single dose of extract from horse-chestnut seeds was 10.6 mg/g of body weight for chicks and 10.7 mg/g of body weight for hamsters. The LD50 for chicks given 2 consecutive daily doses of horse-chestnut seed was 6.5 mg/g. Toxic signs included depression, muscular incoordination, paralysis, coma, and death. Extracts of seeds of Ohio buckeye were nontoxic to chicks and hamsters when fed at 80 mg/g. One of 5 hamsters died after dosing for 5 days with 80 mg/g of extract of seeds of yellow buckeye/g.
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A spontaneously occurring murine renal cystic disease that resembles human adult-onset polycystic renal disease is described. The disease that develops in CFWwd mice is characterized by multiple bilateral cysts in the kidneys in all affected animals and hepatic cysts in approximately 20% of these animals with disease. Occasional thoracic aortic aneurysms were also observed in animals with cystic disease. The prevalence of the disease appears to be determined by the degree of exposure to the ambient environment. A germfree colony of CFWwd mice only rarely displayed the disease, whereas virtually 100% of animals housed for their entire life in the ambient environment died with the disease. Germfree mice removed from the axenic environment and placed in the ambient environment developed the disease, but at a lower prevalence than those animals born and reared in the ambient environment. Disease prevalence in animals reared in environmentally protected caging was between that in germfree and conventional animals. Genetic studies of AKR mice indicated that the disease is inherited in an autosomal dominant fashion but with reduced penetrance.
The purpose of this study was to determine if environmental ammonia is absorbed through the lungs of rats into the blood and, in turn, exerts an effect on blood pH, blood gases, and hepatic drug metabolizing enzyme activity. In phase 1 of the study, rats with surgically implanted aortic cannulas were exposed to varying environmental ammonia concentrations (15 to 1157 ppm). Blood pH, pCO2, pO2, and blood ammonia concentrations were measured at 0, 8, 12, and 24 hours post-exposure. In phase 2, hepatic microsomal enzyme activity (ethylmorphine-N-demethylase and cytochrome P-450) was determined after a 3-day and 7-day exposure to varying environmental ammonia concentrations (4 to 714 ppm). No significant changes were found in blood pH, pCO2, or the histologic appearance of the lungs or trachea. The pO2 and liver microsomal enzymes had only minor changes. The blood ammonia concentration increased significantly (p less than or equal to 0.05) in a linear fashion with increasing environmental ammonia concentrations, indicating pulmonary absorption of ammonia. These levels also declined over time at higher concentrations, suggesting that compensation was occurring. Low environmental ammonia concentrations (less than 100 ppm) produced extremely small changes in blood ammonia concentration, and they had no measurable effects on other parameters examined in the study. These findings suggest that environmental ammonia concentrations found in animal holding rooms may cause minimal adverse effects in healthy rats.
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White Leghorn chickens and mice were orally infected with Trichinella spiralis larvae and their digestive tracts were examined for parasites at postinfection hours (PIH) 5 and 10, and at postinfection days (PID) 1, 2, 4, 6, and 8. Evacuated feces were examined at PIH 5 and 10 and at PID 1, and blood was examined at PID 4, 6, and 8. With the exception of trichinae in the digestive tract (9 at PIH 5 and 2 at PIH 10), parasites were not recovered from chickens. All mice had abundant parasites in the digestive tract and a few parasites in the blood; however, parasites were not found in blood or feces at PID 4. In vitro incubation of infective larvae (4 hours at 37 C) in an extract of glandular stomach or in a combination of extracts from the small intestine, pancreas, and bile of chickens caused visible alterations in 42% to 64% of the larvae and caused total loss of larval infectivity for mice. Sequential incubation in both fluids caused damage in 91% to 97% of the larvae. The same experiments with mouse extracts caused damage in only 8% to 26% of the larvae and infectivity of the larvae for mice was not reduced noticeably. Digestion of infective T spiralis larvae is an important constitutive mechanism of resistance in chickens that probably precludes the transmission of the infection by gallinaceous birds in nature.