title: Host-response patterns of intramammary infections in dairy cows.
abstract: Many different bacterial species have the ability to cause an infection of the bovine mammary gland and the host response to these infections is what we recognize as mastitis. In this review we evaluate the pathogen specific response to the three main bacterial species causing bovine mastitis: Escherichia coli, Streptococcus uberis and Staphylococcus aureus. In this paper we will review the bacterial growth patterns, host immune response and clinical response that results from the intramammary infections. Clear differences in bacterial growth pattern are shown between bacterial species. The dominant pattern in E. coli infections is a short duration high bacteria count infection, in S. aureus this is more commonly a persistent infection with relative low bacteria counts and in S. uberis a long duration high bacteria count infection is often observed. The host immune response differs significantly depending on the invading bacterial species. The underlying reasons for the differences and the resulting host response are described. Finally we discuss the clinical response pattern for each of the three bacterial species. The largest contrast is between E. coli and S. aureus where a larger proportion of E. coli infections cause potentially severe clinical symptoms, whereas the majority of S. aureus infections go clinically unnoticed. The relevance of fully understanding the bovine host response to intramammary infection is discussed, some major gaps in our knowledge are highlighted and directions for future research are indicated.
authors.affiliation: Quality Milk Production Services, Cornell University, 240 Farrier Road, Ithaca, NY 14853, USA. yschukken@cornell.edu
authors.forename: Ynte H
authors.initials: YH
authors.lastname: Schukken
authors.forename: J
authors.initials: J
authors.lastname: Günther
authors.forename: J
authors.initials: J
authors.lastname: Fitzpatrick
authors.forename: M C
authors.initials: MC
authors.lastname: Fontaine
authors.forename: L
authors.initials: L
authors.lastname: Goetze
authors.forename: O
authors.initials: O
authors.lastname: Holst
authors.forename: J
authors.initials: J
authors.lastname: Leigh
authors.forename: W
authors.initials: W
authors.lastname: Petzl
authors.forename: H-J
authors.initials: HJ
authors.lastname: Schuberth
authors.forename: A
authors.initials: A
authors.lastname: Sipka
authors.forename: D G E
authors.initials: DG
authors.lastname: Smith
authors.forename: R
authors.initials: R
authors.lastname: Quesnell
authors.forename: J
authors.initials: J
authors.lastname: Watts
authors.forename: R
authors.initials: R
authors.lastname: Yancey
authors.forename: H
authors.initials: H
authors.lastname: Zerbe
authors.forename: A
authors.initials: A
authors.lastname: Gurjar
authors.forename: R N
authors.initials: RN
authors.lastname: Zadoks
authors.forename: H-M
authors.initials: HM
authors.lastname: Seyfert
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology; D000818:Animals; D002417:Cattle; D016207:Cytokines / Q000276:immunology; D004926:Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D005260:Female; D007111:Immunity, Cellular / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D007774:Lactation / Q000276:immunology; D008321:Mammary Glands, Animal / Q000276:immunology / Q000382:microbiology; D008414:Mastitis, Bovine / Q000276:immunology* / Q000382:microbiology; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D013211:Staphylococcus aureus / Q000276:immunology; D013290:Streptococcal Infections / Q000276:immunology / Q000382:microbiology / Q000662:veterinary; D013291:Streptococcus / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology
chemical_list: D016207:Cytokines; D051193:Toll-Like Receptors