Evaluation of phage therapy in the treatment of Staphylococcus aureus-induced mastitis in mice
Language English Country United States Media print-electronic
Document type Evaluation Study, Journal Article
Grant support
No. 2018YFD0500600
National Key R&D Program of China
Grant No. 201405003
National Public Science and Technology Research Funds Projects of Ocean
PubMed
31256341
DOI
10.1007/s12223-019-00729-9
PII: 10.1007/s12223-019-00729-9
Knihovny.cz E-resources
- MeSH
- Bacteriophages physiology MeSH
- Phage Therapy methods veterinary MeSH
- Mastitis, Bovine microbiology therapy MeSH
- Milk microbiology MeSH
- Myoviridae physiology MeSH
- Mice MeSH
- Podoviridae physiology MeSH
- Cattle MeSH
- Staphylococcal Infections microbiology veterinary MeSH
- Staphylococcus aureus physiology virology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Cattle MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Evaluation Study MeSH
- Geographicals
- China MeSH
Mastitis in dairy cows is generally considered to be the most expensive disease for dairy farmers worldwide. The overuse of antibiotics is a major problem in the treatment of bovine mastitis, and bacteriophage therapy is expected to provide an alternative treatment. The primary aim of this study was to evaluate the efficacy of a phage cocktail against mastitis in a mouse model. First, a Staphylococcus aureus strain was isolated from milk samples taken from mastitis cows from dairy farms in Xinjiang, China, and it was designated as Sau-XJ-21. Next, two phages (designated as vBSM-A1 and vBSP-A2) with strong lytic activity against Sau-XJ-21 were isolated from mixed sewage samples collected from three cattle farms in Xinjiang. Phages vBSM-A1 and vBSP-A2 were identified as members of the Myoviridae and Podoviridae families, respectively. The two phages exhibited a wide range of hosts, especially phage vBSM-A1. To evaluate the effectiveness of the two phages in the treatment against mastitis, female lactating mice were used 10-14 days after giving births. The mice were divided into six groups; one group was kept as healthy control, while the remaining five groups were inoculated with the isolated S. aureus strain to induce mastitis. Four hours after bacterial inoculation, mice in these groups were injected with 25 μL phosphate buffer saline (negative control), ceftiofur sodium (positive control), or phage, either individually or as a cocktail. The mice were sacrificed 20 h later, and the mammary glands were removed and subjected to further analysis, including the quantitation of colony-forming units (CFU), plaque-forming units (PFU), and gross macroscopic as well as histopathology observation. Mice with induced mastitis exhibited significantly improved mastitic pathology and decreased bacterial counts after they had been given phage treatments, with the phage cocktail being more superior than either phage alone. Furthermore, the cocktail treatment also maintained the highest intramammary phage titer without spreading systemically. The effectiveness of the phage cocktail was comparable to that produced by ceftiofur sodium. According to the data obtained for the mouse model of mastitis, phage therapy could be considered as an innovative alternative to antibiotics for the treatment of bovine mastitis.
See more in PubMed
J Dairy Sci. 2007 Jun;90(6):2778-87 PubMed
Front Microbiol. 2017 May 31;8:983 PubMed
Biology (Basel). 2018 Jan 09;7(1): PubMed
Vaccine. 2018 Jun 7;36(24):3513-3521 PubMed
Front Microbiol. 2016 Sep 08;7:1391 PubMed
Front Public Health. 2014 Sep 16;2:145 PubMed
BMJ. 2007 Aug 25;335(7616):389-94 PubMed
Front Microbiol. 2018 Feb 05;9:127 PubMed
Curr Opin Microbiol. 2007 Oct;10(5):461-72 PubMed
Appl Environ Microbiol. 2012 Apr;78(7):2297-305 PubMed
Food Microbiol. 2017 Apr;62:141-146 PubMed
Curr Opin Microbiol. 2005 Aug;8(4):480-7 PubMed
Lancet Infect Dis. 2005 Feb;5(2):115-9 PubMed
PLoS One. 2015 Jan 23;10(1):e0116571 PubMed
Trends Microbiol. 2009 Feb;17(2):66-72 PubMed
Microbiology. 2005 Jul;151(Pt 7):2133-2140 PubMed
Curr Protein Pept Sci. 2012 Dec;13(8):699-722 PubMed
Pancreas. 1998 Apr;16(3):312-5 PubMed
Cal West Med. 1929 Jul;31(1):5-10 PubMed
Infect Immun. 2005 Dec;73(12):7932-7 PubMed
J Appl Microbiol. 2009 Jul;107(1):1-13 PubMed
Crit Care. 2017 Jun 4;21(1):129 PubMed
J Dairy Sci. 2018 Jun;101(6):5531-5548 PubMed
Appl Environ Microbiol. 2015 Oct 16;82(1):87-94 PubMed
Fish Shellfish Immunol. 2016 Jul;54:302-11 PubMed
Respir Res. 2006 Jul 12;7:98 PubMed
J Dairy Sci. 2010 Apr;93(4):1551-60 PubMed
mBio. 2012 Mar 06;3(2):e00029-12 PubMed
Vet Q. 2006 Mar;28(1):2-13 PubMed
Viruses. 2017 Mar 18;9(3): PubMed
J Dairy Sci. 2017 Nov;100(11):8796-8803 PubMed
Vet Res Commun. 2018 Sep;42(3):243-250 PubMed
Microbes Infect. 2005 Mar;7(3):560-8 PubMed
Curr Pharm Biotechnol. 2010 Jan;11(1):69-86 PubMed
Arterioscler Thromb Vasc Biol. 2011 May;31(5):1001-6 PubMed
Clin Exp Med. 2009 Dec;9(4):303-12 PubMed
J Inflamm (Lond). 2018 Mar 22;15:5 PubMed
Curr Microbiol. 2016 Apr;72(4):377-82 PubMed
Bacteriophage. 2011 Mar;1(2):66-85 PubMed
Clin Otolaryngol. 2009 Aug;34(4):349-57 PubMed
Arch Immunol Ther Exp (Warsz). 1999;47(5):267-74 PubMed
Clin Infect Dis. 2011 Feb 15;52(4):481-4 PubMed
J Clin Microbiol. 2012 Mar;50(3):688-95 PubMed
J Med Microbiol. 1970 May;3(2):273-82 PubMed
Curr Pharm Biotechnol. 2010 Jan;11(1):28-47 PubMed
Nat Biotechnol. 2005 Apr;23(4):445-51 PubMed
Sci Rep. 2018 May 1;8(1):6845 PubMed
J Dairy Sci. 2018 Jun;101(6):4729-4746 PubMed
Nat Rev Microbiol. 2010 May;8(5):317-27 PubMed
Front Microbiol. 2017 Nov 28;8:2348 PubMed
Appl Environ Microbiol. 2011 Mar;77(6):2042-50 PubMed
Appl Microbiol Biotechnol. 2019 Jun;103(11):4279-4289 PubMed
Annu Rev Microbiol. 1950;4:21-34 PubMed