Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, spherical bacteria, alpha-hemolytic member of the genus Streptococcus. S. pneumoniae cells are usually found in pairs (diplococci) and do not form spores and are non motile. As a significant human pathogenic bacterium S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century, and is the subject of many humoral immunity studies. Streptococcus pneumoniae resides asymptomatically in healthy carriers, typically colonizing the respiratory tract, sinuses, and nasal cavity. However, in susceptible individuals with weaker immune systems, such as the elderly and young children, the bacterium may become pathogenic and spread to other locations to cause disease. It spreads by direct person-to-person contact via respiratory droplets and by auto-inoculation in persons carrying the bacteria in their upper respiratory tracts. It can be a cause of neonatal infections. Streptococcus pneumoniae is the main cause of community acquired pneumonia and meningitis in children and the elderly, and of sepsis in those infected with HIV. The organism also causes many types of pneumococcal infections other than pneumonia. These invasive pneumococcal diseases include bronchitis, rhinitis, acute sinusitis, otitis media, conjunctivitis, meningitis, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscess.
Streptococcus pneumoniae can be differentiated from the viridans streptococci, some of which are also alpha-hemolytic, using an optochin test, as S. pneumoniae is optochin-sensitive. S. pneumoniae can also be distinguished based on its sensitivity to lysis by bile, the so-called "bile solubility test". The encapsulated, Gram-positive, coccoid bacteria have a distinctive morphology on Gram stain, lancet-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 100 different serotypes are known , and these types differ in virulence, prevalence, and extent of drug resistance. The capsular polysaccharide (CPS) serves as a critical defense mechanism against the host immune system. It composes the outermost layer of encapsulated strains of S. pneumoniae and is commonly attached to the peptidoglycan of the cell wall. It consists of a viscous substance derived from a high-molecular-weight polymer composed of repeating oligosaccharide units linked by covalent bonds to the cell wall. The virulence and invasiveness of various strains of S. pneumoniae vary according to their serotypes, determined by their chemical composition and the quantity of CPS they produce. Variations among different S. pneumoniae strains significantly influence pathogenesis, determining bacterial survival and likelihood of causing invasive disease. Additionally, the CPS inhibits phagocytosis by preventing granulocytes' access to the cell wall.
History In 1881, the organism, known later in 1886 as the pneumococcus for its role as a cause of pneumonia, was first isolated simultaneously and independently by the U.S. Army physician George Sternberg and the French chemist Louis Pasteur. The organism was termed Diplococcus pneumoniae from 1920 because of its characteristic appearance in Gram-stained sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to streptococci. Streptococcus pneumoniae played a central role in demonstrating that genetic material consists of DNA. In 1928, Frederick Griffith demonstrated transformation of life, turning harmless pneumococcus into a lethal form by co-inoculating the live pneumococci into a mouse along with heat-killed virulent pneumococci. In 1944, Oswald Avery, Colin MacLeod, and Maclyn McCarty demonstrated that the transforming factor in Griffith's experiment was not protein, as was widely believed at the time, but DNA. Avery's work marked the birth of the molecular era of genetics.
Genetics The genome of S. pneumoniae is a closed, circular DNA structure that contains between 2.0 and 2.1 million base pairs depending on the strain. It has a core set of 1553 genes, plus 154 genes in its virulome, which contribute to virulence, and 176 genes that maintain a noninvasive phenotype. Genetic information can vary up to 10% between strains. The pneumococcal genome is known to contain a large and diverse repertoire of antimicrobial peptides, including 11 different lantibiotics.
Transformation Natural bacterial transformation involves the transfer of DNA from one bacterium to another through the surrounding medium. Transformation is a complex developmental process requiring energy and depends on the expression of numerous genes. In S. pneumoniae, at least 23 genes are required for transformation. For a bacterium to bind, take up, and recombine exogenous DNA into its chromosome, it must enter a special physiological state called competence. Competence in S. pneumoniae is induced by DNA-damaging agents such as mitomycin C, fluoroquinolone antibiotics (norfloxacin, levofloxacin and moxifloxacin), and topoisomerase inhibitors. Transformation protects S. pneumoniae against the bactericidal effect of mitomycin C. Michod et al. summarized evidence that induction of competence in S. pneumoniae is associated with increased resistance to oxidative stress and increased expression of the RecA protein, a key component of the recombinational repair machinery for removing DNA damage. Based on these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damage. S. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocytes) to produce an oxidative burst that is potentially lethal to the bacteria. The ability of S. pneumoniae to repair oxidative DNA damage in its genome caused by this host defense likely contributes to the pathogen's virulence. Consistent with this premise, Li et al. reported that, among different highly transformable S. pneumoniae isolates, nasal colonization fitness and virulence (lung infectivity) depend on an intact competence system.
Infection
… excerpt ends here. Continue reading the full article.
