Capsule-Negative Staphylococcus aureus Induces Chronic Experimental Mastitis in Mice

Abstract

Staphylococcus aureus capsular polysaccharides (CP) have been shown to enhance staphylococcal virulence in numerous animal models of infection. Although serotype 5 CP (CP5) and CP8 predominate among S. aureus isolates from humans, most staphylococcal isolates from bovines with mastitis in Argentina are capsule negative. This study was designed to evaluate the effects of CP5 and CP8 expression on the pathogenesis of experimental murine mastitis. Lactating mice were challenged by the intramammary route with one of three isogenic S. aureus strains producing CP5, CP8, or no capsule. Significantly greater numbers of acapsular mutant cells were recovered from the infected glands 12 days after bacterial challenge compared with the encapsulated strains. Histopathological analyses revealed greater polymorphonuclear and mononuclear leukocyte infiltration and congestion in the mammary glands of mice infected with the encapsulated strains compared with the acapsular mutant, and the serotype 5 strain elicited more inflammation than the serotype 8 strain. In vitro experiments revealed that the acapsular S. aureus strain was internalized by MAC-T bovine epithelial cells in significantly greater numbers than the CP5-or CP8-producing strain. Taken together, the results suggest that S. aureus lacking a capsule was able to persist in the murine mammary gland, whereas encapsulated strains elicited more inflammation and were eliminated faster. Loss of CP5 or CP8 expression may enhance the persistence of staphylococci in the mammary glands of chronically infected hosts.

Biofilm Formation byStreptococcus pneumoniae: Role of Choline, Extracellular DNA, and Capsular Polysaccharide in Microbial Accretion

“…Furthermore, our observations are in keeping with previous findings reporting that exopolysaccharides influence initial attachment either positively or negatively, depending upon the exopolysaccharide type and the organism (62). This may be the case for S. aureus, which without a capsule was able to better persist in the murine mammary gland (71). However, it is premature to discard the possibility that capsular polysaccharide is not an essential component of biofilm matrix, as recently illustrated in the case of S. aureus, in which biofilm-associated protein (Bap) appears to replace the sugar matrix as a cementing material (68).…”

Characterization of a New Variant of IS 257 That Has Displaced the Capsule Genes within Bovine Isolates of Staphylococcus aureus

“…We showed with an animal model of murine mastitis that a mutant S. aureus strain lacking capsule expression persisted in higher numbers in the infected mammary gland than isogenic CP5-or CP8-producing strains (26). The capsular polysaccharide-negative S. aureus mutant was also internalized in vitro within bovine epithelial cells in greater numbers than the encapsulated strains.…”

Existence of two groups of Staphylococcus aureus strains isolated from bovine mastitis based on biofilm formation, intracellular survival, capsular profile and agr-typing

“…Therefore, the bacteria are not only protected from the action of commonly used antibiotics in mastitis treatment (mainly b-lactams), and also able to persist in the host without causing any apparent inflammation (Boulanger et al, 2003;Garzoni and Kelley, 2009). The absence of capsular expression enhance the adherence to and the invasion of eukaryotic cells by S. aureus (PohlmannDietze et al, 2000;Buzzola et al, 2007;Tuchscherr et al, 2005). In addition, S. aureus bacteria that do not express capsule induce chronic mastitis in mice, suggesting that the absence of capsule synthesis may help the bacteria to persist in the mammary glands (Tuchscherr et al, 2005).…”

“…The absence of capsular expression enhance the adherence to and the invasion of eukaryotic cells by S. aureus (PohlmannDietze et al, 2000;Buzzola et al, 2007;Tuchscherr et al, 2005). In addition, S. aureus bacteria that do not express capsule induce chronic mastitis in mice, suggesting that the absence of capsule synthesis may help the bacteria to persist in the mammary glands (Tuchscherr et al, 2005). Finally, agr group I is associated with a persistence or with features that help the bacteria to persist in the udder: strains belonging to agr group I are more likely to be internalised in epithelial cells, to persist in murine mammary glands (Buzzola et al, 2007) and to be associated with penicillin resistance (Melchior et al, 2011) than the strains belonging to the other groups.…”