title: Mammary Gland Pathology Subsequent to Acute Infection with Strong versus Weak Biofilm Forming Staphylococcus aureus Bovine Mastitis Isolates: A Pilot Study Using Non-Invasive Mouse Mastitis Model.
abstract: BACKGROUND
  Biofilm formation by Staphylococcus aureus is an important virulence attribute because of its potential to induce persistent antibiotic resistance, retard phagocytosis and either attenuate or promote inflammation, depending upon the disease syndrome, in vivo. This study was undertaken to evaluate the potential significance of strength of biofilm formation by clinical bovine mastitis-associated S. aureus in mammary tissue damage by using a mouse mastitis model.
  
  
  METHODS
  Two S. aureus strains of the same capsular phenotype with different biofilm forming strengths were used to non-invasively infect mammary glands of lactating mice. Biofilm forming potential of these strains were determined by tissue culture plate method, ica typing and virulence gene profile per detection by PCR. Delivery of the infectious dose of S. aureus was directly through the teat lactiferous duct without invasive scraping of the teat surface. Both bacteriological and histological methods were used for analysis of mammary gland pathology of mice post-infection.
  
  
  RESULTS
  Histopathological analysis of the infected mammary glands revealed that mice inoculated with the strong biofilm forming S. aureus strain produced marked acute mastitic lesions, showing profuse infiltration predominantly with neutrophils, with evidence of necrosis in the affected mammary glands. In contrast, the damage was significantly less severe in mammary glands of mice infected with the weak biofilm-forming S. aureus strain. Although both IL-1β and TNF-α inflammatory biomarkers were produced in infected mice, level of TNF-α produced was significantly higher (p<0.05) in mice inoculated with strong biofilm forming S. aureus than the weak biofilm forming strain.
  
  
  CONCLUSIONS
  This finding suggests an important role of TNF-α in mammary gland pathology post-infection with strong biofilm-forming S. aureus in the acute mouse mastitis model, and offers an opportunity for the development of novel strategies for reduction of mammary tissue damage, with or without use of antimicrobials and/or anti-inflammatory compounds for the treatment of bovine mastitis.
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.|College of Veterinary Sciences and Animal Husbandry, Central Agricultural University, Selesih, Aizawl, Mizoram, India.
authors.forename: Jully
authors.initials: J
authors.lastname: Gogoi-Tiwari
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Vincent
authors.initials: V
authors.lastname: Williams
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.|Department of Medicine and Cell Biology, Albert Einstein College of Medicine, Bronx, New York, United States of America.
authors.forename: Charlene Babra
authors.initials: CB
authors.lastname: Waryah
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Paul
authors.initials: P
authors.lastname: Costantino
authors.affiliation: School of Pharmacy, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Hani
authors.initials: H
authors.lastname: Al-Salami
authors.affiliation: School of Pharmacy, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Sangeetha
authors.initials: S
authors.lastname: Mathavan
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Kelsi
authors.initials: K
authors.lastname: Wells
authors.affiliation: School of Veterinary and Life Sciences, Murdoch University, Perth, Western Australia, Australia.
authors.forename: Harish Kumar
authors.initials: HK
authors.lastname: Tiwari
authors.affiliation: Ella Foundation, Genome Valley, Hyderabad, India.
authors.forename: Nagendra
authors.initials: N
authors.lastname: Hegde
authors.affiliation: Veterinary College, Karnataka Veterinary, Animal and Fisheries Sciences University, Bangalore, India.
authors.forename: Shrikrishna
authors.initials: S
authors.lastname: Isloor
authors.affiliation: School of Pharmacy, University of Otago, Dunedin, New Zealand.
authors.forename: Hesham
authors.initials: H
authors.lastname: Al-Sallami
authors.affiliation: School of Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, Western Australia, Australia.
authors.forename: Trilochan
authors.initials: T
authors.lastname: Mukkur
mesh_terms: D000818:Animals; D018441:Biofilms / Q000254:growth & development*; D002417:Cattle; D004195:Disease Models, Animal; D005260:Female; D053583:Interleukin-1beta / Q000378:metabolism; D008321:Mammary Glands, Animal / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D008414:Mastitis, Bovine / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D010865:Pilot Projects; D013203:Staphylococcal Infections / Q000382:microbiology* / Q000473:pathology; D013211:Staphylococcus aureus / Q000254:growth & development* / Q000378:metabolism / Q000472:pathogenicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha