Table of Contents
Autolysin (peptidoglycan hydrolase)
Autolysin is a cell wall degrading enzyme that has the ability to enzymatically disrupt and disintegrate S.
Immunoglobulin A1 (IgA1) is the predominant immunoglobulin isotype involved in the protection of mucosal membranes of the upper respiratory tract in humans. IgA1 proteases of S.
A number of other human pathogens such as Haemophilus
Pneumolysin is a pore-forming toxin of 53 kDa composed of 471 amino acids produced by virtually all clinical isolates of the pneumococcus. At high concentration (above 50 hemolytic units), it lyses all cells having cholesterol (receptor for this toxin) on its surface e.g. it damages respiratory epithelium.
Pneumolysin also may cause a range of effects, including induction of apoptosis, activation of host complement, and induce pro-inflammatory reactions in immune cells.
Polysaccharide capsule completely encloses the cell of Streptococcus
- all clinical isolates of S. pneumoniae causing invasive disease are encapsulated;
- loss of the capsule by either genetic mutation or enzymatic degradation dramatically reduces S. pneumoniae virulence in animal models of infection
- different capsular serotypes vary in the ability to cause invasive disease
The capsule may inhibit complement activity (capsule impaired bacterial opsonization with C3b/iC3b by both the alternative and classical complement pathways and also inhibited conversion of C3b bound to the bacterial surface to iC3b) and phagocytosis. The capsule also prevents mechanical removal by mucus and reduce exposure to antibiotics
For S. pneumoniae strains, there are >93 antigenically distinct capsular serotypes and antibody to the polysaccharide capsule provides type-specific immunity.
Pneumococcal wall teichoic acid is involved in pneumococcal infection of sepsis and adherence to epithelial and endothelial cells. Pneumococcal wall teichoic acid enhances pneumococcal colonization and dissemination.
Other virulence factors of S.pneumoniae includes pneumococcal surface protein A (PspA); protection against the complement system, neuraminidase; (which may enhance colonization due to its action on glycans), and pneumococcal surface antigen A, etc.
References and Further Reading
- Streptococcus pneumoniae: virulence factors and variation
- Pneumococcal Virulence Factors: Structure and Function
- LytA, Major Autolysin of Streptococcus pneumoniae, Requires Access to Nascent Peptidoglycan
- The Streptococcus pneumoniae Capsule Inhibits Complement Activity and Neutrophil Phagocytosis by Multiple Mechanisms