Product Code Database
Streptococcus pneumoniae, or pneumococcus, is a Gram-positive, spherical bacteria, alpha-hemolytic member of the genus Streptococcus. (2025). 9780838585290, McGraw Hill. ISBN 9780838585290 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 nasopharynx. However, in susceptible individuals with weaker immune systems, such as the elderly and young children, the bacterium may become 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, coccus bacteria have a distinctive morphology on Gram stain, scalpel-shaped diplococci. They have a polysaccharide capsule that acts as a virulence factor for the organism; more than 100 different 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 , determining bacterial survival and likelihood of causing invasive disease. Additionally, the CPS inhibits phagocytosis by preventing ' access to the cell wall.
The organism was termed Diplococcus pneumoniae from 1920 because of its characteristic appearance in Gram stain sputum. It was renamed Streptococcus pneumoniae in 1974 because it was very similar to Streptococcus.
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.
S. pneumoniae undergoes spontaneous phase variation, changing between transparent and opaque colony phenotypes. The transparent phenotype has a thinner capsule and expresses large amounts of phosphorylcholine (ChoP) and choline-binding protein A (CbpA), contributing to the bacteria's ability to adhere and colonize in the nasopharynx. The opaque phenotype is characterized by a thicker capsule, resulting in increased resistance to host clearance. It expresses large amounts of capsule and pneumococcal surface protein A (PspA) which help the bacteria survive in the blood. Phase-variation between these two phenotypes allows S. pneumoniae to survive in different human body systems.
While a few different bacterial infections can lead to meningitis, S. pneumoniae is one of the leading causes of this infection. Pneumococcal meningitis occurs when the bacteria goes from the blood to the central nervous system, which is made up of the brain and the spinal cord. Here, the infection will spread and cause inflammation, leading to severe disabilities like brain damage or hearing loss or limb removal or death. Symptoms include common problems such as head aches, fevers, and nausea, but the more telling signs that a bacterial infection may have reached the brain are sensitivity to light, seizures, having limited range in neck movement, and easy bruising all over the body.
Osteomyelitis, or bone infection, is a rare occurrence but has been seen in patients who were diagnosed to have a S. pneumoniae infection that went untreated for too long.
Sepsis is caused by overwhelming response to an infection and leads to tissue damage, organ failure, and even death. The symptoms include confusion, shortness of breath, elevated heart rate, pain or discomfort, over-perspiration, fever, shivering, or feeling cold.
Less severe illnesses that can be caused by pneumococcal infection are conjunctivitis (pink eye ), otitis media (middle ear infection), Bronchitis (airway inflammation), and sinusitis (sinus infection).
Currently, there are two vaccines available for S. pneumoniae: the pneumococcal polysaccharide vaccine (PPV23) and the pneumococcal conjugate vaccine (PCV13). PPV23 functions by utilizing CPS to stimulate the production of type-specific antibodies, initiating processes such as complement activation, opsonization, and phagocytosis to combat bacterial infections. It elicits a humoral immune response targeting the CPS present on the bacterial surface. PPSV23 offers T cell-independent immunity and requires revaccination 5 years after the first vaccination because of its temporary nature. PCV13 was developed when determining its low efficacy in children and infants. PCV13 elicits a T-cell-dependent response and provides enduring immunity by promoting interaction between B cell and T cells, leading to an enhanced and prolonged immune response.
The recent advances in next-generation sequencing and comparative genomics have enabled the development of robust and reliable molecular methods for the detection and identification of S. pneumoniae. For instance, the Xisco gene was recently described as a biomarker for PCR-based detection of S. pneumoniae and differentiation from closely related species.
Atromentin and leucomelone possess antibacterial activity, inhibiting the enzyme enoyl-acyl carrier protein reductase, (essential for the biosynthesis of ) in S. pneumoniae.
|
|
