scholarly journals Production of Antibodies in Egg Whites of Chickens

Author(s):  
Angel Justiz Vaillant ◽  
Belkis Ferrer-Cosme ◽  
Sehlule Vuma

Background:  IgM, which participates in the primary immune response, is the primary antibody in egg whites. There is scant information about the production of antibodies in egg whites. This study describes the preparation of antibodies against a bacterial antigen, staphylococcal protein-A. Methods: The detection of antibodies against staphylococcal protein-A in egg white was performed by ELISA, and the antibodies were purified by protein-A affinity chromatography. Agglutination inhibition of Staphylococcus aureus Cowan I strains by purified antibodies against protein-A in vitro was investigated. Results:  ELISA showed the production of antibodies against staphylococcal protein-A in the egg whites of layer hens. The antibodies were separated using affinity chromatography. The agglutination of Staphylococcus aureus Cowan I strains occurred when the purified antibodies were incubated with S. aureus. Conclusion: The results showed that it is possible to produce antibodies against bacterial antigens in egg whites, which can have industrial applications in the preparation of antibodies for immunotherapy of infectious diseases.

2017 ◽  
Vol 80 (3) ◽  
pp. 476-481 ◽  
Author(s):  
V. Murugadas ◽  
C. Joseph Toms ◽  
Sara A. Reethu ◽  
K. V. Lalitha

ABSTRACT Methicillin-resistant Staphylococcus aureus (MRSA) has been a global health concern since the 1960s, and isolation of this pathogen from food-producing animals has been increasing. However, little information is available on the prevalence of MRSA and its clonal characteristics in seafood and the aquatic environment. In this study, 267 seafood and aquatic environment samples were collected from three districts of Kerala, India. Staphylococcal protein A (spa) typing and multilocus sequence typing (MLST) was performed for 65 MRSA strains isolated from 20 seafood and aquatic environment samples. The MRSA clonal profiles were t657-ST772, t002-ST5, t334-ST5, t311-ST5, t121-ST8, t186-ST88, t127-ST1, and two non-spa assignable strains. Whole spa gene sequence analysis along with MLST confirmed one strain as t711-ST6 and another as a novel MRSA clone identified for the first time in seafood and the aquatic environment with a t15669 spa type and a new MLST profile of ST420-256-236-66-82-411-477. The MRSA strains were clustered into five clonal complexes based on the goeBURST algorithm, indicating high diversity among MRSA strains in seafood and the aquatic environment. The novel clone formed a separate clonal complex with matches to three loci. This study recommends large-scale spa typing and MLST of MRSA isolates from seafood and the aquatic environment to determine the prevalence of new MRSA clones. This monitoring process can be useful for tracing local spread of MRSA isolates into the seafood production chain in a defined geographical area.


Author(s):  
Yao Hu ◽  
Wen Zhou ◽  
Chengguang Zhu ◽  
Yujie Zhou ◽  
Qiang Guo ◽  
...  

Smoking is considered a key risk factor for implant survival; however, how it interacts with the pathogens in peri-implant infections is not clear. Here, we identified that nicotine, the key component of cigarette smoking, can interact with Staphylococcus aureus and synergistically induce peri-implant infections in a rat osteolysis model. The nicotine–S. aureus combination group increased the gross bone pathology, osteolysis, periosteal reactions, and bone resorption compared to the nicotine or S. aureus single treated group (p < 0.05). Nicotine did not promote the proliferation of S. aureus both in vitro and in vivo, but it can significantly upregulate the expression of staphylococcal protein A (SpA), a key virulence factor of S. aureus. The nicotine–S. aureus combination also synergistically activated the expression of RANKL (receptor activator of nuclear factor-kappa B ligand, p < 0.05) to promote the development of peri-implant infections. The synergistic effects between nicotine and S. aureus infection can be a new target to reduce the peri-implant infections.


1985 ◽  
Vol 153 (3) ◽  
pp. 579-585 ◽  
Author(s):  
Bengt GUSS ◽  
Karen LEANDER ◽  
Ulf HELLMAN ◽  
Mathias UHLEN ◽  
John SJOQUIST ◽  
...  

2020 ◽  
Author(s):  
Yi-Chien Lee ◽  
Pao-Yu Chen ◽  
Jann-Tay Wang ◽  
Shan-Chwen Chang

Abstract Background: Fosfomycin exhibits excellent in vitro activity against multidrug-resistant pathogens, including methicillin-resistant Staphylococcus aureus (MRSA). Increasing fosfomycin resistance among clinical MRSA isolates was reported previously, but little is known about the genetic mechanisms of fosfomycin resistance.Methods: All MRSA isolates, collected in 2002 and 2012 by the Taiwan Surveillance of Antimicrobial Resistance (TSAR) program, were used in this study. Susceptibility to various antimicrobial agents, including fosfomycin, was determined by broth microdilution. Genetic determinants of fosfomycin resistance, including fosB carriage and murA, glpT and uhpT mutations, were investigated using PCR and sequencing of amplicons. Staphylococcal protein A (spa) typing was also performed to determine the genetic relatedness of MRSA isolates.Results: A total of 969 MRSA strains, 495 in the year 2002 and 474 in the year 2012, were analyzed. The overall in vitro susceptibility was 8.2% to erythromycin, 18.0% to clindamycin, 29.0% to tetracycline, 44.6% to ciprofloxacin, 57.5% to trimethoprim/sulfamethoxazole, 86.9% to rifampicin, 92.9% to fosfomycin and 100% to linezolid and vancomycin. A significant increase in the fosfomycin resistance rate was observed from 3.4% in 2002 to 11.0% in 2012. Of 68 fosfomycin-resistant MRSA isolates, 12 harbored the fosB gene, and expression of murA, uhpT, and glpT mutations was noted in 11, 59, and 66 isolates, respectively. Combination of mutations of uhpT and glpT genes (58 isolates) was the most prevalent resistant mechanism. The vast majority of the fosfomycin-resistant MRSA isolates belonged to spa type t002.Conclusions: An increased fosfomycin resistance rate of MRSA isolates was observed in our present study, mostly due to mutations in the glpT and uhpT genes. Clonal spread probably contributed to the increased fosfomycin resistance.


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