by Robert Ballough
Streptococcus pneumoniae is found worldwide. The common host is the human body, in which it often does not cause disease but at other times it can cause diseses in particular, pneumonia. It also causes otitis media, bacteremia, meningitis, peritonitis, and sinusitis. The route by which this organism is spread is from human to human in the form of aerosol droplets. When inside the host the organism’s primary site of pneumococcal colonization is the nasopharynx. From this site it can aspire to the lungs, eventually spread to the blood and traverse the blood-brain barrier to the meninges, once inside the blood it can cause infections throughout the body. Symptoms of the disease include sudden chill, fever, cough, pleuritic pain, or sputum with a red/brown rusty color.
Streptococcus pneumoniae is a gram-positive coccus. Usually they are found in pairs of cocci, or diplococci, but they may also occur in short chains or singly. When cultured on blood agar they demonstrate alpha hemolysis. They are non motile organisms.
Virulence is caused by the chemical composition of the capsule. There are over 90 serotypes of S. pneumoniae which causes great difficulty when trying to develop a vaccine for this bacterium. The capsule interferes with phagocytosis by preventing C3b opsonization of the bacterial cells.
S. pneumoniae is the leading cause of pneumonia in all ages. Pneumonia due to this organism is characterized by four stages. In the first stage the lung alveoli fill up with a serous fluid which is thought to be stimulated by the cell wall of the organism. This fluid contains a lot of organisms but little inflammatory cells. The spread of the organism throughout the lungs is mediated by this fluid. In the second stage, neutrophils, which are attracted by the S. pneumoniae and there chemotactic signals and the host cell’s alternate pathway, invade the alveoli. Also red blood cells are recruited to this site. In the third stage, mostly neutrophils are packed into the alveoli and very few bacteria remain. In the final stage, macrophages eliminate the remaining residue from the inflammatory response. As one can see, the damage which is done to the lung is largely a result of the host’s inflammatory response, which causes the build up of fluids in the lungs. If S. pneumoniae is allowed to persist in the lungs it can then invade the blood, which causes bacteremia. When in the blood it can traverse the blood-brain barrier and infect the meninges, which results in meningitis. S. pneumoniae is also associated with diseases in other parts of the respiratory tract including the paranasal sinuses, which is better known as sinusitis, and the middle ear can become infected, which is known as otitis media. It has also been known to cause peritonitis, an inflammation of the peritoneum, the membrane that lines the abdominal wall, and it is also implicated in causing arthritis.
A gram stain is performed from the sputum of the infected patient. The presence of neutrophils and greater than ten gram-positive diplococci usually results in the diagnosis of Streptococcus pneumoniae. For further conformation of this organism, it is streaked on blood agar. When on blood agar the organism should exhibit alpha-hemolysis, which is characterized as a zone of green coloring around the colonies of bacteria on the agar. This test isn’t always 100 percent conclusive because other Streptococcus bacteria can cause alpha-hemolysis. Therefore, the streaked organisms must also exhibit bile or optochin sensitivity to have greater assurance that this organism is in fact S. pneumoniae.
There are several different treatment options for S. pneumoniae infections. For severe pneumococcal infections penicillin G is used. For mild pneumococcal infections penicillin V is used. Due to a growing number of penicillin resistant S. pneumoniae this organism has become a greater concern. S. pneumoniae has a natural transformation system in which genetic material is exchanged between two organisms. Therefore, bacteria that have developed antibiotic resistance, whether due to mutation or natural selection, can often pass these traits to other bacteria. This natural transformation is accelerated by the fact that these bacteria have a relatively fast growth rate and achieve large cell densities in an infectious setting. Because of these natural attributes the spread of the antibiotic resistant genes is cause for great concern. Fortunately, Erythromycin has been shown to work well on these penicillin resistant bacteria. For the prevention of this disease, a vaccine is currently offered which has a 23-valent capsular polysaccharide which protects against the most common strains, but due to the great antigenic variety of the S. pneumoniae, which has at least 90 different strains, a universal vaccine cannot be developed.
S. pneumoniae most commonly inflicts children, the elderly, and other people with weakened immune systems. The incidence among adults exhibits a midwinter peak and a striking dip in the summer, due to closer living conditions during the winter. Up until 2000, S. pneumoniae infections caused 100,000-135,000 hospitalizations for pneumonia, 6 million cases of otitis media, and 60,000 cases of invasive disease, which included 3300 cases of meningitis. Incidence in the U.S. showed geographic variation from 21 to 33 cases per 100,000 people. Interestingly enough, Alaska native adults have an 8 times higher disease rate and Alaskan infants a 4 times higher rate than the benchmark U.S. community. This statistic is indicative of how the organism is spread, because S. pneumoniae is spread by aerosol droplets, from person to person. The fact that Alaskan’s must remain indoors and live in crowded conditions and poor ventilated homes, increases the transmission and therefore the incidence of S. pneumoniae in this area.