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Pathogen Page

Streptococcus pneumoniae

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Pneumonia

3. Introduction

Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, alpha-hemolytic diplococcus aerotolerant anaerobe and a member of the genus Streptococcus. S. pneumoniae is the most common cause of both pneumonia overall and fatal pneumonia. Antibiotic resistance has developed worldwide and is most frequent in pneumococcal serotypes that are most prevalent in children (types/groups 6, 14, 19, and 23). The incidence of pneumococcal disease is the highest in children < 2 years of age and in adults > 65 years of age. Other important risk factors are chronic heart and lung disease, cigarette smoking, and asplenia (Ortqvist et al., 2005). Other than pneumonia, it also causes acute sinusitis, otitis media, meningitis, bacteremia, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.

4. Microbial Pathogenesis

S. pneumoniae is normally found in the nasopharynx. It attaches to nasopharyngeal cells through interaction of bacterial surface adhesins. It can cause otitis media or sinusitis if it enters areas such as the Eustachian tube or nasal sinuses. Pneumonia occurs if the organisms are inhaled into the lungs and not eliminated. S. pneumoniae can activate complement, stimulate cytokine production, and attracts neutrophils and other white blood cells. The organism's polysaccharide capsule makes it resistant to phagocytosis. S. pneumoniae can spread to other areas and cause various diseases. S. pneumoniae has several virulence factors, including the polysaccharide capsule, pneumococcal surface proteins, and IgA1 protease (Wiki: S. pneumoniae).

5. Host Ranges and Animal Models

Pneumococci spontaneously cause disease in humans, monkeys, rabbits, horses, mice and guinea pigs. Nasopharyngeal colonization occurs in approximately 40% of the population (Textbook of Bacteriology).

6. Host Protective Immunity

The bacteria invade and grow primarily due to their resistance to the host phagocytic response. The cell wall components directly activate multiple inflammatory cascades, including the alternative pathway of complement activation, the coagulation cascade and the cytokine cascade, inducing interleukin-1, interleukin-6 and tumor necrosis factor (TNF) from macrophages and other cells (Textbook of Bacteriology).

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