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Biomedical subjects

D G Brownstein

Publications and source records attributed to D G Brownstein.

At least 55 records · Page 3Linked to original sources
PubMed1984

Experimental Lyme disease in rabbits: spirochetes found in erythema migrans and blood.

In attempts to produce experimental Lyme disease, 33 rabbits were inoculated with Lyme spirochetes by tick feeding or from tick organ homogenates or cultures. Two rabbits developed erythema chronicum migrans at the site of inoculation, in one instance 2 days after injection of a tick organ homogenate and in the other instance, 17 days after feeding of infected Ixodes dammini ticks. Spirochetes were seen in skin biopsy specimens of the second lesion with Warthin-Starry and immunoperoxidase stains. Spirochetes were also recovered from blood cultures of two additional rabbits 2 weeks post-inoculation. These findings are characteristic of early Lyme disease in humans and give additional support for the spirochetal etiology of Lyme disease.

Animals↗
PubMed1984

Spontaneous Reye's-like syndrome in BALB/cByJ mice.

In five spontaneous outbreaks, sixty-four BALB/cByJ mice developed Reye's-like syndrome 4 to 33 days after introduction into mouse rooms known to harbor a variety of indigenous murine viruses. The clinical course lasted 24 hours and consisted of progressively deteriorating consciousness and hyperventilation, usually leading to death. Mice killed and necropsied while stuporous or comatose had serum ammonia levels of 2524 +/- 179 versus 66 +/- 8 micrograms/dl for control BALB/cByJ mice. Necropsy findings included swollen, diffusely pale yellow livers with panlobular microvesicular fatty change, pale renal cortices with epithelial fat droplets of the proximal convoluted tubules, and Alzheimer type II astrocytosis of the neocortex, corpus striatum, hippocampus, and thalamus. In three of the five outbreaks involving 66% of affected animals, mice had active coronaviral enteritis. Electron microscopic changes in hepatocytes, neocortical astrocytes, and neurons were similar to or identical with those described for the acute phase of Reye's syndrome in man. The epizootiology of these outbreaks and the apparent synchrony between Reye's syndrome-like illness and the stage of intestinal coronavirus infections in some of these outbreaks suggest that one or more naturally occurring murine viruses were of etiologic significance.

Animal Diseases↗
PubMed1984

Response of weanling random-bred mice to infection with pneumonia virus of mice (PVM).

Weanling random bred mice inoculated intranasally with 2,500 median tissue culture infectious doses of pneumonia virus of mice (PVM) had recoverable virus in the upper respiratory tract for the first 9 days post-infection. Virus was isolated from the lungs only on day 5. Seroconversion was first detected on day 9, and serum antibody titers continued to rise throughout the period of the study (24 days). Lesions were confined to the nasal cavity of infected mice. Susceptible contacts placed in cages with infected mice did not seroconvert to PVM.

Animals↗
PubMed1983

Genetics of natural resistance to Sendai virus infection in mice.

The genetics of resistance to a naturally occurring respiratory infection caused by Sendai virus was examined in F1, F2, and backcross progeny of resistant C57BL/6J and susceptible DBA/2J mice and in 25 recombinant inbred strains. An intranasal inoculum of 0.1 50% tissue culture infective dose (low dose) of Sendai virus caused 0% mortality in C57BL/6J and F1 mice and 73% mortality in DBA/2J mice. An inoculum of 1.0 50% tissue culture infective dose (high dose) caused 3, 0, and 89% mortality in C57BL/6J, F1, and DBA/2J mice, respectively. Low-dose infection caused 36% mortality in F1 X DBA/2J hybrids and 0% mortality in F2 hybrids. High-dose infection caused 29 and 32% mortality in F1 X DBA/2J and F2 hybrids, respectively. Resistance was not linked to H-2 haplotype, coat color, or sex. High-dose infection caused deaths in 12 recombinant inbred strains, and the strain distribution pattern was concordant with that of a chromosome 1 marker, Sas-1, in 20 of 25 strains (P less than 0.01). Resistance therefore behaved as a simple Mendelian dominant trait which presumptively mapped to chromosome 1.

Animals↗
PubMed1983

Genetics of dystrophic epicardial mineralization in DBA/2 mice.

The genetics of dystrophic epicardial mineralization in mice was studied using 6 to 8-week-old hybrids and recombinant inbred strains derived from DBA/2J (high prevalence) and C57B1/6J (low prevalence) mice. DBA/2J mice of both sexes were uniformly affected. No cases were seen among 32 F1 mice and 82 F2 mice. Six out of 31 backcross progeny obtained from F1 females backcrossed to DBA/2J males were affected. Two out of 25 recombinant inbred strains were affected. These results suggest that dystrophic epicardial mineralization is determined by three or four unlinked autosomal recessive alleles.

Animals↗
PubMed1983

The induction of liver tumors by 239Pu citrate or 239PuO2 particles in the Chinese hamster.

The influence of radiation dose distribution on the frequency of 239Pu-induced liver tumors was evaluated in the Chinese hamster. Different concentrations of 239Pu citrate 239PuO2 particles of known sizes were injected intravenously via the jugular vein. About 60% of the injected 239Pu citrate was deposited in the liver and 40% in the bone. The 239Pu citrate was rather uniformly distributed throughout the liver parenchyma. Injected plutonium oxide particles were taken up by the reticuloendothelial system with 90% of the body burden deposited in the liver. The 239PuO2 particles were localized in the Kupffer cells and produced nonuniform dose distributions that were dependent on particle size. There was an activity- and dose-dependent increase in the incidence of total liver parenchymal cell tumors following injection with either plutonium particles or citrate. For animals that received 14.0-, 2.7-, 0.3-, and 0.04-Gy dose to liver from 239Pu citrate the cumulative tumor incidence was 39, 32, 5, and 0%, respectively. Animals that were injected with the 0.24 micron 239PuO2 particles had doses of 42.0, 7.2, and 0.8 Gy to the liver and tumor incidences of 34, 26, and 5%, respectively. Plutonium citrate also produced hemangiosarcomas of the liver and tumors in bone and bone marrow. The latent period for liver tumor appearance in animals exposed to 239Pu citrate or 239PuO2 particles increased as the injected activity decreased. For animals injected with a similar total activity (7.4 Bq/g), the lifetime cumulative liver tumor incidence was similar for animals exposed to either 239Pu citrate (32%) or 239PuO2 (26%). There was little effect of particle size on liver tumor incidence. These data indicate that, in Chinese hamster liver, local radiation dose distribution is less important in altering tumor incidence than injected activity or average dose. However, the more uniform irradiation from 239Pu citrate administration was more effective in cancer production than the nonuniform irradiation from 239PuO2 particles.

Alpha Particles↗
PubMed1982

Experimental nasal infection of normal and leukopenic mice with Pseudomonas aeruginosa.

Histological and ultrastructural changes in the nasal mucosa of normal and leukopenic mice exposed to Pseudomonas aeruginosa were compared and correlated with changes in the distribution of pseudomonads by use of immunoperoxidase labeling. Pseudomonas was limited to the surface of the nasal mucosa of normal mice and was cleared rapidly. Concurrently, granulocytes were recruited across unaltered nasal epithelium and contained phagocytosed bacilli within two hours. Pseudomonas was limited to the surface of the nasal mucosa of most leukopenic mice at two hours. By four hours, pseudomonads had penetrated interepithelial junctions of all leukopenic mice. Granulocytes were not recruited and nasal epithelium underwent necrosis at points of invasion. These results show that neutrophils participate in the clearance of P. aeruginosa from the surface of the nasal mucosa and that the failure to recruit granulocytes may be important in the breakdown of epithelial barriers. Possible mechanisms of mucosal invasion are discussed.

Animals↗
PubMed1982

Mouse hepatitis virus immunofluorescence in formalin- or Bouin's-fixed tissues using trypsin digestion.

Mouse hepatitis viral antigens were demonstrated by immunofluorescence in formalin- and Bouin's-fixed tissues processed routinely for histopathology followed by partial digestion with trypsin. Staining was superior in tissues fixed in formalin and was not diminished in tissue sections from paraffin blocks stored at room temperature as long as 2 years. The relative ease of this procedure and the commercial availability of reagents makes this a useful technique for the definitive diagnosis of mouse hepatitis virus infection.

Acetates↗
PubMed1981

Sendai virus infection in genetically resistant and susceptible mice.

The pathogenesis of Sendai virus infection in genetically resistant (C57Bl/6) and susceptible (DBA/2) nonimmune adult mice was investigated. Rising serum complement-fixation (CF) antibody titers were delayed in DBA/2 mice as compared with C57Bl/6 mice. C57Bl/6 mice developed descending desquamative endobronchiolitis, and DBA/2 mice developed descending proliferative endobronchiolitis and bronchogenic alveolitis. Peribronchiolar lymphoid cuffs that formed in C57Bl/6 mice were thicker and more densely populated than those of DBA/2 mice. Immunofluorescence demonstrated viral antigens confined to the epithelial lining of conducting airways in C57Bl/6 mice but extending to alveolar corner cells in DBA/2 mice. Studies with a transmission electron microscope confirmed that Type II pneumocytes were infected only in DBA/2 mice. IgG-containing cells selectively accumulated along the airways of both strains, but fewer were recruited by DBA/2 mice. These results suggest that genetic resistance to Sendai virus is expressed through the immune system.

Animals↗
PubMed1980

Spontaneous endomyometrial neoplasms in aging Chinese hamsters.

Twenty-one endomyometrial neoplasms among 93 nulliparous noninbred Chinese hamsters were evaluated. The median survival time of the 93 females was 1,040 days. The median age of hamsters with endomyometrial neoplasms was 1,200 days. Neoplasms were classified as carcinoma or malignant mixed müllerian tumors of the endometrium and benign or malignant myometrial neoplasms. There were 13 endometrial adenocarcinomas. Three tumors were mixed adenosquamous carcinomas, which occurred in significantly older Chinese hamsters than did adenocarcinomas. Three malignant mixed müllerian tumors consisted of 2 carcinosarcomas and 1 mixed mesodermal tumor. The 2 myometrial neoplasms were a leiomyoma and a leiomyosarcoma. The classification and relative frequency of these neoplasms were similar to endomyometrial neoplasms of women, which makes Chinese hamsters useful subjects for studies of spontaneous endomyometrial cancers.

Adenocarcinoma↗
PubMed1980

Immunology of the lower respiratory tract. Serial morphologic changes in the lungs and tracheobronchial lymph nodes of dogs after intrapulmonary immunization with sheep erythrocytes.

Sequential histologic changes in immunized and contralateral lung lobes, and ipsilateral and contralateral tracheobronchial lymph nodes were evaluated from dogs after intra-pulmonary immunization with sheep erythrocytes. In addition, changes in the relative numbers of unstimulated lymphocytes, activated lymphocytes, and plasma cells were determined for immunized and contralateral lung lobes by the use of bronchopulmonary lavage. Histologic evidence of an immune response occurred 2 days after immunization in ipsilateral tracheobronchial lymph nodes and on Day 5 in immunized lung lobes. Pulmonary lymphoid infiltrates appeared initially around pulmonary venules and veins. There was expansion of these infiltrates into alveolar spaces, where mixed mononuclear aggregates were formed in association with alveolar macrophages 7 days after immunization. A similar but attenuated and delayed response occurred within contralateral control lung lobes, although mononuclear aggregates were not found. Activated lymphocytes in lavage samples increased prior to histologic evidence of pulmonary lymphoid infiltrates. These results suggest that after intrapulmonary immunization the lung recruits circulating immunocytes produced in ipsilateral lung-associated lymph nodes as the source of specific antibody-forming cells in bronchoalveolar air spaces.

Animals↗
PubMed1980

Reflex-mediated desquamation of bronchiolar epithelium in guinea pigs exposed acutely to sulfuric acid aerosol.

Terminal conducting airways are known to be vulnerable to direct injury by a variety of noxious aerosols. Sulfuric acid aerosol, a by-product of fossil fuel combustion, produces desquamation of terminal bronchiolar epithelium in guinea pigs that is believed to result from direct deep lung irritation, an effect separable from reflex airway constriction induced by sulfuric acid. To characterize desquamation of bronchiolar epithelium, 20 guinea pigs were exposed to 32.6 mg/cu m sulfuric acid aerosol with a mass median aerodynamic diameter of 1.0 micron for 4 hours. The guinea pigs were killed upon termination of the exposure, or 24 hours later, and airway alterations were evaluated by light and transmission electron microscopy. To test whether the development of bronchiolar epithelial desquamation is independent of reflex airway constriction, 24 guinea pigs were exposed to an identical aerosol for 4 hours after pretreating half with 5 mg/kg atropine sulfate intraperitoneally to inhibit airway constriction. Sulfuric acid produced diffuse pulmonary hyperinflation with areas of consolidation and atelectasis. Epithelial desquamation occurred in airways supplying regions of developing atelectasis and was most extensive in terminal bronchioles. Parasympathetic effector blockade with atropine eliminated epithelial desquamation. These results indicate that sulfuric acid-produced desquamation of terminal bronchiolar epithelium is not separable from reflex airway constriction and that terminal conducting airways are vulnerable not only to direct injury by noxious aerosols but also to indirect, reflex-mediated injury.

Aerosols↗
PubMed1980

Acute parvoviral enteritis in a closed beagle dog colony.

An outbreak of acute canine parvoviral enteritis occurred over 2 months in a closed beagle dog research colony containing approximately 1840 dogs. Of the 183 puppies housed in the whelping kennel, the morbidity and mortality were 36% and 12%, respectively. Four cases occurred in the adult population with three deaths. The disease was characterized clinically by anorexia, diarrhea, rapid dehydration, and panleukopenia. It was more prevalent in weaned puppies than in nursing puppies or adult dogs.

Acute Disease↗
PubMed1979

Toxicity of 0.4- and 0.8-microm sulfuric acid aerosols in the guinea pig.

To determine mortality caused by inhaled sulfuric acid mist, groups of Hartley guinea pigs 2-3 mo old were exposed for 8 h to graded concentrations of aerosols of 0.4 or 0.8 microm mass median aerodynamic diameter. Relative humidity during exposures was maintained at 70-80%. Based on probit analysis, the concentration required to produce 50% mortality (LC50) for deaths to 21 d after exposure was 30 mg/m3 for the 0.8-microm aerosol. For the 0.4-microm aerosol, the LC50 was above 109 mg/m3, the highest concentration obtainable at that particle size. At both particle sizes, the animals either tended to develop severe dyspnea and die minutes (0.4 microm) or hours (0.8 microm) thereafter or appeared nearly unaffected. Lesions in animals that died as a results of 0.4-microm exposures were restricted to hyperinflation; animals that died as a result of 0.8-microm exposures also showed hemorrhage and transudation. No gross or histopathologic changes were observed in animals that appeared unaffected during exposure. Differences in total and/or regional respiratory tract deposition may account for the different responses to the two aerosols.

Aerosols↗
PubMed1979

Chronic active hepatitis in dogs associated with leptospires.

Chronic active hepatitis was diagnosed in five American Foxhounds from one kennel. Spirochetes were demonstrated in the liver in four of the dogs. A rising titer to Leptospira interrogans serovar grippotyphosa was found in the fifth dog, although spirochetes were not demonstrated in tissues. A serologic survey at the kennel revealed evidence of exposure of 6 of 13 dogs to grippotyphosa. This is the first report of an association between chronic active hepatitis leptospiral infection in any species.

Animals↗
PubMed1978

Pathogenesis of bacteremia due to Pseudomonas aeruginosa in cyclophosphamide-treated mice and potentiation of virulence of endogenous streptococci.

Mice treated with cyclophosphamide on day 0 were killed at sequential intervals during subsequent administration of Pseudomonas aeruginosa in drinking water and were examined for sites of bacterial colonization and multiplication with use of peroxidase-labeled antibody and culture techniques. These studies were coordinated with those of clinical and histopathologic changes. Bacterial antigen was first detected on day 4 on the surface of nasal squamocolumnar junctions and the stratum corneum of gingival sulci and crests. Invasion of tissue by P. aeruginosa proceeded rapidly from these sites and led to bacteremia. There was no invasion of the lower alimentary canal. Endogenous group B beta-hemolytic streptococci colonized and penetrated ulcers created by previous pseudomonas invasion. These results suggest that epithelial colonization is the critical event in the pathogenesis of bacteremia due to P. aeruginosa in the immunosuppressed host. The resulting infection may provide a conduit for invasion and enhancement of the virulence of endogenous streptococci.

Animals↗
PubMed1977

Cryptosporidium in snakes with hypertrophic gastritis.

Fourteen captive snakes of three genera and four species had severe chronic hypertrophic gastritis. Persistent postprandial regurgitation and firm midbody swelling were the most common clinical signs. Fecal smears had many roughly spherical organisms confirmed by ultrastructural study to be oocysts of Cryptosporidium. Pathologic changes included hypertrophy of gastric mucosa and atrophy of granular cells. There were cystic changes in gastric glands and focal mucosal necrosis. Many Cryptosporidium lined microvillar surfaces. All developmental forms were identified by ultrastructure. Characteristic oocysts were found in abundance.

Animals↗