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Failure Of The Congo Red Dye Uptake Test To Discriminate Between Virulent And Avirulent Avian Escherichia Coli, Kathy R. Spears, Richard E. Wooley, John Brown, Lisa K. Nolan
Failure Of The Congo Red Dye Uptake Test To Discriminate Between Virulent And Avirulent Avian Escherichia Coli, Kathy R. Spears, Richard E. Wooley, John Brown, Lisa K. Nolan
Lisa K. Nolan
Twenty avian Escherichia coli isolates from normal and diseased chickens were compared by use of three virulence tests. These tests included the uptake of Congo red dye, an embryo lethality test, and a quantitative microtiter complement resistance test. A direct correlation was seen between the results of the complement resistance test and the embryo lethality test. The results of the Congo red test did not correlate with the two other tests.
Identification And Prevalence Of A Genetic Defect That Causes Leukocyte Adhesion Deficiency In Holstein Cattle, Dale E. Shuster, Marcus E. Kehrli Jr., Mark R. Ackermann, R. O. Gilbert
Identification And Prevalence Of A Genetic Defect That Causes Leukocyte Adhesion Deficiency In Holstein Cattle, Dale E. Shuster, Marcus E. Kehrli Jr., Mark R. Ackermann, R. O. Gilbert
Mark R. Ackermann
Two point mutations were identified within the gene encoding bovine CD18 in a Holstein calf afflicted with leukocyte adhesion deficiency (LAD). One mutation causes an aspartic acid to glycine substitution at amino acid 128 (D128G) in the highly conserved extracellular region of this adhesion glycoprotein, a region where several mutations have been found to cause human LAD. The other mutation is silent. Twenty calves with clinical symptoms of LAD were tested, and all were homozygous for the D128G allele. In addition, two calves homozygous for the D128G allele were identified during widespread DNA testing, and both were subsequently found to …
Relationship Of Complement Resistance And Selected Virulence Factors In Pathogenic Avian Escherichia Coli, Richard E. Wooley, Kathy R. Spears, John Brown, Lisa K. Nolan, Oscar J. Fletcher
Relationship Of Complement Resistance And Selected Virulence Factors In Pathogenic Avian Escherichia Coli, Richard E. Wooley, Kathy R. Spears, John Brown, Lisa K. Nolan, Oscar J. Fletcher
Lisa K. Nolan
Complement resistance, antibiotic resistance profiles, and virulence profiles of 80 Escherichia coli isolates from the intestines of normal chickens (40 isolates) and chickens diagnosed as having colisepticemia (40 isolates) were compared. Differences were observed between the two groups for antibiotic resistance, siderophore production, presence of type 1 pili, complement resistance, motility, and size of plasmids. The systemic isolates were more likely to have siderophores and type 1 pili, and to be complement-resistant and motile than were the intestinal isolates. No differences between the two groups were observed for colicin production. Further comparison of the 10 most complement-resistant isolates from the …
Characteristics Of Conjugative R-Plasmids From Pathogenic Avian Escherichia Coli, Richard E. Wooley, Kathy R. Spears, Lisa K. Nolan, John Brown, Mark A. Dekich
Characteristics Of Conjugative R-Plasmids From Pathogenic Avian Escherichia Coli, Richard E. Wooley, Kathy R. Spears, Lisa K. Nolan, John Brown, Mark A. Dekich
Lisa K. Nolan
Three of four virulent avian Escherichia coli isolates transferred a single large molecular-weight R-plasmid to two recipient E. coli strains. Antibiotic resistances transferred included streptomycin (two isolates) and streptomycin-tetracycline-sulfa (one isolate). Production of colicin and siderophores, complement resistance, and embryo lethality present in the virulent isolates were not transferred to recipient organisms. From the results, it appears that the R-plasmids of these virulent avian E. coli are not associated with virulence.
Animal Model Of Human Disease: Bovine Leukocyte Adhesion Deficiency: Beta2 Integrin Deficiency In Young Holstein Cattle, Marcus E. Kehrli Jr., Mark R. Ackermann, Dale E. Shuster, Martin J. Van Der Maaten, Frank C. Schmalstieg, Donald C. Anderson, Bonnie J. Hughes
Animal Model Of Human Disease: Bovine Leukocyte Adhesion Deficiency: Beta2 Integrin Deficiency In Young Holstein Cattle, Marcus E. Kehrli Jr., Mark R. Ackermann, Dale E. Shuster, Martin J. Van Der Maaten, Frank C. Schmalstieg, Donald C. Anderson, Bonnie J. Hughes
Mark R. Ackermann
Leukocyte adhesion deficiency (LAD), is a rare, autosomal recessive disorder caused by a lack or partial absence of a family of leukocyte integrins, Mac-1, LFA-1, and p150,95.1 The leukocyte (32) integrins are glycoproteins essential for normal leukocyte-endothelial cell adherence and emigration. Affected children develop recurrent bacterial infections, persistent leukocytosis, severe hypoplasia of lymphoid tissues and isolated neutrophils, eosinophils, macrophages, and lymphocytes have abnormal function when tested in vitro. Most patients without bone marrow transplants die at an early age.
Use Of Rats To Compare Atrophic Rhinitis Vaccines For Protection Against Effects Of Heat-Labile Protein Toxin Produced By Pasteurella Multocida Serogroup D, J. R. Thurston, R. B. Rimler, Mark R. Ackermann, N. F. Cheville
Use Of Rats To Compare Atrophic Rhinitis Vaccines For Protection Against Effects Of Heat-Labile Protein Toxin Produced By Pasteurella Multocida Serogroup D, J. R. Thurston, R. B. Rimler, Mark R. Ackermann, N. F. Cheville
Mark R. Ackermann
Four bacterin-toxoid and three bacterin commercial vaccines against atrophic rhinitis were tested in rats for their capacity to immunize against the lethal and systemic effects of purified heat-labile protein toxin (D-toxin) produced by Pasteurella multocida serogroup D. Only one bacterin-toxoid vaccine stimulated sufficient immunity to prevent the death of all rats challenged with D-toxin. None of the vaccines prevented weight loss, leukocytosis or increases in serum complement titers in rats challenged with D-toxin. Rats provide an inexpensive animal model for testing the capacity of vaccines to generate antitoxic immunity against the lethal and systemic effects of D-toxin.
Comparison Of A Complement Resistance Test, A Chicken Embryo Lethality Test, And The Chicken Lethality Test For Determining Virulence Of Avian Escherichia Coli, Lisa K. Nolan, Richard E. Wooley, John Brown, Kathy R. Spears, H. W. Dickerson, Mark Dekich
Comparison Of A Complement Resistance Test, A Chicken Embryo Lethality Test, And The Chicken Lethality Test For Determining Virulence Of Avian Escherichia Coli, Lisa K. Nolan, Richard E. Wooley, John Brown, Kathy R. Spears, H. W. Dickerson, Mark Dekich
Lisa K. Nolan
Results with four pathogenic avian Escherichia coli isolates and one avirulent isolate in a complement resistance test, a chicken lethality test, and a chicken embryo lethality test were compared. Results of the complement resistance test with these isolates were highly correlated to results of the chicken lethality test of virulence. The chicken embryo test yielded results that were of a medium positive correlation with the chicken lethality results. The results of the complement resistance and chicken embryo lethality tests were highly correlated.
Transposon Mutagenesis Used To Study The Role Of Complement Resistance In The Virulence Of An Avian Escherichia Coli Isolate, Lisa K. Nolan, Richard E. Wooley, Richard K. Cooper
Transposon Mutagenesis Used To Study The Role Of Complement Resistance In The Virulence Of An Avian Escherichia Coli Isolate, Lisa K. Nolan, Richard E. Wooley, Richard K. Cooper
Lisa K. Nolan
The role of complement resistance in the virulence of an avian Escherichia coli isolate was examined with transposon mutagenesis. A suicide plasmid containing a kanamycin-encoding mini-transposon was used to transform a virulent complement-resistant avian E. coli isolate. A less resistant mutant was identified that contained a transposon insertion in a plasmid and in the chromosome. This loss of complement resistance was associated with a drop in virulence in an embryo assay. No other phenotypic changes were detected in the mutant. These results suggest that complement resistance is associated with the virulence of this organism.
Intestinal Adenocarcinoma Of The Ileocecal Junction In A Chicken, James R. Andreasen Jr., Claire B. Andreasen
Intestinal Adenocarcinoma Of The Ileocecal Junction In A Chicken, James R. Andreasen Jr., Claire B. Andreasen
Claire B. Andreasen
An 89-week-old male chicken was presented with signs of depression, emaciation, and weakness. At necropsy, a stricture was found at the ileocecal junction that resulted in blockage and dilation of the ileum proximal to the stricture. Histologically, neoplastic epithelial cells that contained mucin had invaded the intestinal wall and produced a fibrous connective tissue reaction. The lesion was diagnosed as scirrhous intestinal adenocarcinoma.
Light Microscopic And Ultrastructural Pathology Of Seminiferous Tubules Of Rats Given Multiple Doses Of Pasteurella Multocida Group D Protein Toxin, Mark R. Ackermann, James P. Tappe Jr., John R. Thurston, Richard B. Rimler, Dale E. Shuster, Norman F. Cheville
Light Microscopic And Ultrastructural Pathology Of Seminiferous Tubules Of Rats Given Multiple Doses Of Pasteurella Multocida Group D Protein Toxin, Mark R. Ackermann, James P. Tappe Jr., John R. Thurston, Richard B. Rimler, Dale E. Shuster, Norman F. Cheville
Mark R. Ackermann
Male Holtzman rats were given subcutaneous doses of a purified Pasteurella multocida group D heat-labile toxin on alternate days for up to 22 days. Rats were necropsied at 18 days or 36 days (14 days after last dose of toxin) or when moribund, and testicles were taken for histologic and ultrastructural examination. Other selected tissues, including liver and spleen, were taken for histologic examination. Histologically, testicular and splenic lesions occurred more consistently and at much smaller doses when compared with lesions in other target organs such as liver. Testicular and splenic lesions were present in all rats (6/6) given 0.8 …