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Histopathology and pathogenesis of mouse mastitis induced with Staphylococcus aureus mutants
Abstract:
Mammary glands of mice were inoculated with a well-defined strain of Staphylococcus aureus or with derived mutants lacking alpha-haemolysin, coagulase or protein A, in order to evaluate the pathogenicity of these factors. Alpha-haemolysin-negative and coagulase-negative mutants showed less virulence than the wild-type strain. Various protein A-negative mutants gave contradictory results. The lesions ranged from consistently non-reactive necrosis of the entire mammary gland to a limited inflammatory reaction. The necroses, especially when affecting the whole mammary gland, were mostly associated with vascular lesions. Because the necroses were non-reactive, the vascular lesions were considered to be primary, but they could not be linked exclusively with the effect of alpha-haemolysin and a multifactorial aetiology seemed most probable. After inoculation with coagulase-lacking bacteria the development of parenchymal lesions was delayed, hypothetically because of increased phagocytic activity. The investigation indicated that protein A could have influenced the pathogenesis of the lesions, since all but one of the mutants lacking protein A showed low virulence, whereas a high protein A-producing, haemolysin-negative mutant was as virulent as the wild-type strain. A connection between protein A, bacterial adherence and bacterial growth rate is therefore conceivable. The possibility cannot be excluded, however, that during mutagenesis some as yet unknown cell surface factors were affected.
Insights
Staphylococcus aureus virulence factors like alpha-haemolysin and coagulase contribute to pathogenicity in mouse mammary glands. Protein A also appears to influence disease development, though its role is complex.
Area of Science:
- Microbiology
- Pathogenesis
- Bacterial Virulence Factors
Background:
- Staphylococcus aureus is a significant pathogen causing various infections.
- Understanding the specific roles of virulence factors is crucial for developing targeted treatments.
- Mammary gland infections by S. aureus can lead to significant pathology.
Purpose of the Study:
- To investigate the pathogenicity of Staphylococcus aureus virulence factors: alpha-haemolysin, coagulase, and protein A.
- To determine the contribution of these factors to the development of mammary gland lesions in mice.
Main Methods:
- Inoculation of mouse mammary glands with wild-type Staphylococcus aureus and its derived mutants lacking specific virulence factors.
- Histopathological examination of mammary gland lesions, including necrosis and inflammation.
- Assessment of bacterial virulence based on lesion severity and host response.
Main Results:
- Alpha-haemolysin-negative and coagulase-negative mutants exhibited reduced virulence compared to the wild-type strain.
- Coagulase-deficient mutants showed delayed parenchymal lesion development, potentially due to enhanced phagocytosis.
- Protein A-negative mutants displayed varied virulence, suggesting a role for protein A in pathogenesis, possibly linked to bacterial adherence and growth.
- Vascular lesions were identified as primary contributors to necrosis, with a likely multifactorial etiology.
Conclusions:
- Alpha-haemolysin and coagulase are important virulence factors for Staphylococcus aureus in mammary gland infections.
- Protein A likely plays a role in S. aureus pathogenesis, influencing lesion development.
- The pathogenesis of S. aureus-induced mammary gland lesions is multifactorial, potentially involving unknown cell surface factors.