Relationship of Hydrogen Peroxide Production by Mycoplasma pulmonis to Virulence for Catalase-deficient Mice

Abstract

Mycoplasma pulmonis, an etiological agent of murine pneumonia, produced about 0.065 ,umoles of hydrogen peroxide (H202) per hr per 1010 colony-forming units. When glucose was present at a concentration of 0.01 M, H202 production was increased by 50%. To determine if H202 production by M. pulmonis could be correlated with virulence, normal, acatalasemic, and acatalatic mice were infected with the organism. Three days after infection with M. pulmonis significantly more acatalatic mice had pneumonia than did normal or acatalasemic mice. The pneumonia in acatalatic mice was also more severe than in the other two groups. Five days after infection, pneumonia in the acatalatic mice was resolved, whereas normal mice were severely affected. The presence of pneumonia and the severity were correlated with the recovery of M. pulmonis from the lesions. In vitro studies of the effect of catalase on M. pulmonis showed that exogenously supplied catalase stimulated the growth of M. pulmonis at 37 C and prolonged its survival at 25 C. Hemolysis of sheep blood, guinea pig blood, rabbit blood, and normal and acatalasemic mouse blood by M. pulmonis was inversely related to the catalase activity of the erythrocytes. These findings suggest that H202 secretion contributes to the virulence of M. pulmonis and to the death of the microorganism in the absence of host catalase.

Trypsin-sensitive, bovine serum albumin-dependent hemolysis activity in Mycoplasma pulmonis

“…Although several Mycoplasma species, including M. pulmonis (6), produce peroxides (2,6,19) with hemolytic activity, the catalase-insensitive hemolysis reported above clearly results from some other mechanism. This activity is unusual in that it affects only RBCs in which the membrane surface has been made more accessible by removal or increased diffusion of glycophorin.…”

The mycoplasmas.

“…42,1978 ogenic M. hyorhinis and A. granularum (224), and loss of virulence in M. pneumoniae was not accompanied by a decrease in H202 production (165). As will be discussed at length later, the bulk of the H202 produced by mycoplasmas in an animal is quickly destroyed by the host catalase and peroxidase activities unless the host is genetically devoid of these enzymes, such as acatalatic mice (29). For the H202 to exert its toxic effect, the mycoplasmas must adhere close enough to the host cell surface to maintain a toxic, steady-state concentration of H202 sufficient to cause direct damage to the cell membrane, such as by lipid peroxidation (46).…”

Role of innate immunity in respiratory mycoplasma infection

“…Likewise, hydrogen peroxide, the end product of respiration in mycoplasmas, may act as a virulence factor, but the loss of virulence for M. pneumoniae does not correlate to decreased hydrogen peroxide production (79). Catalase deficient mice infected with M. pulmonis developed more severe pneumonia earlier but managed to clear the infection faster than immunocompetent controls (80). These data suggest that while hydrogen peroxide production may be important for the establishment of infection, host catalase ultimately controls oxygen radical production and prevents damage to the mycoplasmas.…”