Catalase, superoxide dismutase, and virulence of Staphylococcus aureus. In vitro and in vivo studies with emphasis on staphylococcal--leukocyte interaction.

Abstract

A B S T R A C T Since oxygen-free polymorphonuclear neutrophils (PMN) cannot kill Staphylococcus aureus normally, the usual mechanisms for PMN bactericidal activity probably involve hydrogen peroxide or superoxide. Catalase can destroy hydrogen peroxide, and superoxide dismutase breaks down superoxide. Experiments were performed to study the influence of these enzymes (which are found in staphylococci) on virulence for mice or on leukocyte-bacterial interaction. 15 staphylococcal strains were injected i.p. into mice to quantitate virulence. There was good correlation between staphylococcal catalase activity and mouse lethality (r = 0.88) but no correlation between staphylococcal superoxide dismutase activity and mouse lethality (r = 0.14). Exogenous catalase (10,000 U/ml) increased the virulence of low-catalase staphylococci, but exogenous superoxide dismutase (200 izg/ml) did not alter the virulence of staphyloccal strains. C14-labeled high-catalase or low-catalase staphylococci were ingested equally well by PMN, with or without the addition of exogenous catalase. A high-catalase staphylococcal strain was killed relatively poorly by PMN, and addition of exogenous catalase (but not superoxide dismutase) decreased the ability of PMN to kill a low-catalase strain. Iodination of bacterial proteins by PMN is related to hydrogen peroxide, and a high-catalase staphylococcal strain was iodinated only 63% as much as a low-catalase Portions of this work were presented at the National

Catalase (KatA) and Alkyl Hydroperoxide Reductase (AhpC) Have Compensatory Roles in Peroxide Stress Resistance and Are Required for Survival, Persistence, and Nasal Colonization inStaphylococcus aureus

“…KatA was described as a major virulence determinant in S. aureus, but studies with a catalase mutant revealed no difference in virulence in a murine abscess model of infection (34,18). We have shown compensatory expression and activity of AhpC in the absence of KatA.…”

“…Thus, scavenging of H 2 O 2 is important for aerobic survival. Catalase (KatA) is known to detoxify H 2 O 2 and was proposed to be a major virulence determinant in Staphylococcus aureus (34), where strains producing low levels of KatA were more sensitive to killing by neutrophils. However, a katA mutant of S. aureus was not attenuated in a murine-abscess model of infection (17).…”

Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models

“…Catalase has traditionally been implicated as a virulence determinant in S. aureus (Kanafani & Martin, 1985;Mandell, 1975). However, recent studies with S. aureus katA mutants have revealed no differences in virulence from the corresponding wild-type strains in murine models of infection (Cosgrove et al, 2007;Horsburgh et al, 2001).…”

“…Thus, this enzyme has been demonstrated to be an essential factor for the intracellular survival of bacteria such as Mycobacterium tuberculosis (Manca et al, 1999), Campylobacter jejuni (Day et al, 2000) and Helicobacter pylori (Basu et al, 2004). In S. aureus, the role of catalase in virulence remains unclear; while some researchers have observed a correlation between virulence and catalase activity (Kanafani & Martin, 1985;Mandell, 1975), others have not found any evidence of this (Cosgrove et al, 2007;Horsburgh et al, 2001).…”

In vitro resistance of Burkholderia cepacia complex isolates to reactive oxygen species in relation to catalase and superoxide dismutase production

“…SODs of Shigella flexneri (Franzon et al, 1990), Salmonella typhimurium (Fang et al, 1999), Listeria monocytogenes (Welch et al, 1979), Aeromonas salmonicida (Barnes et al, 1996) and Photobacterium damselae (Barnes et al, 1999) have been reported to increase the resistance to killing by oxygen radicals. Catalase activity is thought to protect Staphylococcus aureus (Mandell, 1975), and to a limited extent Shigella flexneri (Franzon et al, 1990), Salmonella typhimurium (Tsolis et al, 1995), Mycobacterium tuberculosis (Manca et al, 1999) and Agrobacterium tumefaciens (Xiu & Pan, 2000).…”