Pneumococcus or pneumococcus, is,, aerotolerant anaerobic member. Significant human, S.
pneumonia was recognized as a major cause in the late 19th century and is the subject of much research
. Despite the name, in the body leads to many types
also. These invasive pneumococcal diseases include,,,,,,,,,,, and. S. pneumonia
is one of the most common causes of bacterial meningitis in adults and adolescents, as well, and is the main cause of bacterial meningitis in adults in the United States. It is also one of the top two isolates found in ear infections, middle ear inflammation. Pneumococcal pneumonia is more common in very young and very old. S. pneumonia
can be distinguished from, some of which are also alpha hemolytic, using test and
,
S. pneumonia is optochin sensitive. S. pneumonia
You can also differentiate on the basis of its sensitivity to lysis of bile (called "Test the solubility of bile.") Encapsulated, gram-positive bacteria
is a different morphology on Gram so-called " lancet-shaped "diplococci. They have a polysaccharide capsule that acts as a virulence factor for the body, more than 90 different serotypes are known, and these types differ in virulence, prevalence and degree of drug resistance. [In 1881 the body known as pneumococcus for its role as an agent of pneumonia, was first isolated at the same time and independently of each other U. S Army doctor
and French chemist. The organism was named dyplokokk pneumonia because of its distinctive look in. It was renamed
pneumoniae in 1974 because of its growth in chains in liquid media. S. pneumonia
plays a central role in the demonstration of genetic material and is. In 1928
revealed life, turning harmless pneumococcus into a deadly form of the joint living pneumococcus vaccine in the mouse with the dead heat,
pneumococci. In 1944, and
demonstrated the transforming factor was DNA, not protein, as was widely believed at the time. The work marked the birth of Avery molecular genetics era. [Genome S. pneumonia
closed, circular structure of DNA, which contains from 2. 0 and 2. 1000000 base pairs, depending on the strain. It has a basic set of 1553 genes and 154 genes in that contribute to virulence, and 176 genes that support non-invasive phenotype. Genetic information can be changed to 10% between strains. S. pneumonia
is part of the normal flora of the upper respiratory tract, but, like many natural flora, it can become pathogenic under the right conditions (for example, if the immune system is suppressed host). Invasins, such as anti >> << capsules, different adhezyny and immunogenic cell wall components, all of the major virulence factors. [[Interaction of Haemophilus influenzae and S. pneumonia as
to be found in the human upper respiratory tract. Research competition
in vitro showed S. pneumonia
overcome H. Influenza
attacking him. When bacteria are both together in the nasal cavity of mice for 2 weeks only
H. Influenza
survives. When the two are separate in the nasal cavity, one survives. After examining the upper respiratory tissues of mice as bacteria, extremely large number
immune cells were detected. In mice, only a single bacteria cell no. Laboratory tests show that neutrophils are already dead H. Influenza
were more aggressive in attacking S. pneumonia
neutrophils than unexposed. Influence killed
H. Influenza
no effect on living H.influenzae. When H. Influenza
attack S.pneumoniae, it signals the immune system to attack
S. pneumonia combination of these two groups of species with the immune system signal that is not installed on any type separately. It is unclear why H. Influenza
does not depend on the immune system. [The diagnosis is usually made based on clinical suspicion, together with positive cultures of specimens from almost anywhere in the body. S. pneumonia
, whole
sensitive strattera prescription, although optochin resistance was observed. and have antibacterial activity by inhibiting the enzyme
(you need to on) in S. pneumonia. [[[.