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Biomedical subjects

L T Patterson

Publications and source records attributed to L T Patterson.

At least 37 records · Page 2Linked to original sources
PubMed1975

The avian inflammatory response: adaptation and utilization of skin windows.

A modified skin window system was developed and utilized for examination of the local inflammatory response in the chicken. Data were collected at 2, 4, 6, 8, 12, 24, 28, 32 and 48 hours following wing-web scarification. The first cells observed were heterophils and they remained the predominant type through 32 hours. Mononuclears began infiltrating at a rapid rate of 8 to 12 hours, and by 48 hours they represented slightly more than one-half of the total cells observed. The total number of cells present increased rapidly to a peak at 24 hours, and then declined during the 24 to 48 hour period. The percentage of heterophils and mononuclears showed an inverse relationship throughout the 48 hour period, as appreciable numbers of eosinophils and basophils were not observed. Macrophages were the predominant mononuclear cells. Degranulation of heterophils was extensive in the 2 to 4 hour periods, but was much less common thereafter. As the time after scarification increased, macrophages exhibited; (1) increased cytoplasm to nucleus ratio, (2) increased numbers of phagocytic vacuoles, and (3) a marked tendency to form giant cells. The results obtained in this study were similar to those recorded for mammals, except that the percentage shift toward mononuclears occurred at a faster rate in mammals.

Animals↗
PubMed1971

Pathological response of the chicken embryo to an agent which causes acute leukosis (Marek's disease).

A laboratory test system specific for Marek's disease was developed by using the pathological response of the chicken embryo. Chicken epidermal scales (dander) and feather calami from infected chickens contain an agent(s) which after a 3- to 4-day incubation period caused gross or microscopic pathological changes (or both) in the embryo. A cell-free inoculum was obtained from infectious dander by 5-min sonic treatment, differential centrifugation, and membrane filtering (0.45 mum). Evidence for the cell-free existence of this agent(s) was obtained when membrane filtrates of dander preparations were shown to cause Marek's disease in 10-day-old chickens and in chickens inoculated at 1 day of age.

Acute Disease↗
PubMed1971

Correlation of immunological responsiveness with lymphocyte changes in chickens infected with Marek's disease.

Several immunological, hematological, and pathological responses associated with Marek's disease were determined. Four-week-old Marek's disease-infected and control chickens were injected with Salmonella pullorum antigen. About one-half of all infected chickens tested were unresponsive to antigenic challenge. Antibody titers in responsive infected chickens were significantly depressed at 1 and 2 weeks post-inoculation when compared to controls. Total white blood cell counts of control and control-antigen chickens were significantly lower than counts in infected chickens. Based on response to antigenic challenge, 24% of the responsive group had leukemia compared to 54% of the unresponsive chickens. The predominant cell populations in these two groups responsible for the mononuclear cell leukemia were large lymphocytes and blast cells. These cell increases were significantly greater in unresponsive chickens. Also, transient increases in the granulocytic elements were observed in some infected chickens. Large fluctuations in hematocrit values were observed in Marek's disease-infected chickens. As many as 30% of the infected chickens were anemic throughout the testing periods. Infected chickens which did not receive antigen had lower incidences of mortality and gross lesions than similarly treated chickens which did receive antigen. In addition, those chickens which were unresponsive to antigenic challenge had a higher mortality rate and increased percentages of gross lesions when compared with responsive chickens.

Agglutination Tests↗
PubMed1968

Association of C-reactive protein and circulating leukocytes with resistance to Staphylococcus aureus infection in endotoxin-treated mice and rabbits.

The response of rabbits and mice to treatment with Escherichia coli endotoxin, as measured by C-reactive protein (CRP) and leukocyte levels, and resistance to Staphylococcus aureus infection was studied to evaluate the significance of these responses and their associations. In both species, there was an initial leukopenia without early recovery of normal lymphocyte levels. This was followed by an increase in polymorphonuclear leukocytes and a return to near the normal range. The CRP level was slightly altered during the stage of decreased resistance and increased throughout the remainder of the period of observation. The resistance level was decreased initially, recovered to normal levels, and continued to increase. The changes in CRP and resistance levels were closely associated. It would appear that this association between CRP and resistance, the antibacterial activity of CRP, and its action on the polysaccharides obtained from bacterial cell walls are evidence for the participation of CRP in nonspecific resistance to infection.

Animals↗
PubMed1965

Mouse C-reactive protein and endotoxin-induced resistance.

Patterson, L. T. (University of Texas, Galveston), and R. D. Higginbotham. Mouse C-reactive protein and endotoxin-induced resistance. J. Bacteriol. 90:1520-1524. 1965.-The relationship between the level of C-reactive protein (CRP) in the sera of mice and resistance to Staphylococcus aureus infection after the injection of Escherichia coli endotoxin was studied. The CRP level was essentially unchanged at 6 hr after endotoxin, and resistance was slightly decreased. At 24 hr after endotoxin, both CRP levels and resistance were increased. Since the increase in the CRP level and resistance appeared to be associated, it was of interest that, when mouse CRP was tested for in vitro reactions with several strains of bacteria, cells of all species of gram-positive bacteria tested (including S. aureus) were agglutinated by CRP. E. coli was not agglutinated under the conditions of the test. It is proposed that mouse CRP is an opsonin, and possibly a lysin, and is involved in nonspecific resistance to infection with S. aureus.

Agglutination Tests↗