Streptococcus pneumoniae: Meningitis

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Scanning Electron Micrograph of Streptococcus pneumonmiae by R. Facklam, J. Carr, Source: CDC.

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Streptococcus pneumoniae is a non-motile, non-spore forming, gram-positive bacteria of the firmicute phylum. S. pneumoniae is also commonly referred to as pneumococcus [1,2]. Streptococcus pneumoniae are in the shape of a slightly pointed coccus. The diameter of each single pneumococcus organism ranges from 0.5 to 1.25 micrometers. S. pneumoniae is found singly and in short chains, but mainly these bacteria are found in pairs (diplococci) [2]. Streptococcus pneumoniae uses fermentation to produce energy via converting glucose into lactic acid. Furthermore, Streptococcus pneumoniae utilizes extracellular enzyme systems in order to obtain carbon and nitrogen, and these processes damage host tissue and permit S. pneumoniae to colonize the host (Todar 2003). Streptococcus pneumoniae and Haemophilus influenzae contribute to the same mucosal microenvironment. Both bacteria are capable of living on their own. But, Lysenko et al. (2005) showed that Haemophilus influenzae swiftly outcompetes Streptococcus pneumoniae when they are in the same environment. Thus, H. influenzae can remove populations of the S. pneumoniae pathogen (Lysenko et al. 2005).

This bacteria exclusively inhabits human beings and are mesophillic, meaning they optimally inhabit areas with temperatures ranging from 30 to 35 degrees Celsius. Streptococcus pneumoniae is most commonly found in the upper respiratory tract, specifically in the nasopharynx (the nasal passages). Most people carry these bacteria in their nasopharynx, and the harboring of S. pneumoniae within a human is called carriage. Even though most people carry these bacteria in their nasopharynx, most of the time S. pneumoniae does not cause disease [1,2].

A polysaccharide capsule encloses the entire S. pneumoniae cell, and this sugar capsule is key to this bacteria’s virulence. There are hundreds of surface proteins on Streptococcus pneumoniae. Choline-binding proteins are an important group of surface proteins expressed by S. pneumoniae, and this group of proteins helps attach the bacteria to human cells (Todar 2003).

Historical Significance

Louis Pasteur was the first person to isolate Streptococcus pneumoniae, although at the time was only known as pneumococcus because it could cause pneumonia in humans. In 1974, this species of bacteria was officially named Streptococcus pneumoniae because it can form chains in liquid.

Streptococcus pneumoniae was a key bacteria in the development of molecular genetics field. Fred Griffith, in 1928, used S. pneumoniae to discover the transformation process in bacteria (Lederberg et al. 2005). In 1944, building off of Griffith’s findings, Avery, MacLeod, and McCarthy demonstrated that DNA and not protein was the genetic material, using the transformative factor in the Streptococcus pneumoniae (Lederberg et al. 2005).


Bacterial infection via S. pneumoniae spreads from person to person by means of respiratory droplets. Transmission typically occurs when a carrier coughs or sneezes within six feet of other potentially infected people. Carriers are normally healthy, however, these carriers have the potential to be a source of infection for others [1].

Infection and Spread

Although S. pneumoniae can be harmless at low cell densities, when the concentration of this bacteria increases too high in its host it can cause infection [2]. Streptococcus pneumoniae can radiate from the nasopharynx to other parts of the body and cause infection and disease there. Streptococcus pneumoniae can cause a wide range of illnesses, including: otitis media (ear infection), sinusitis (sinus infection), bacteraemia (blood infection), pneumonia (lung infection), arthritis, and peritonitis (peritoneum infection, thin tissue lining the walls of the abdomen). Furthermore, S. pneumoniae can infect the lining of the brain and spinal cord, which are normally bacteria-free. Infection in this sterile area leads to meningitis. When Streptococcus pneumoniae infects these sterile areas it is then referred to as ‘invasive’ pneumococcal disease, which can result in serious complications or death [1].

Until 2000, Pneumoniae streptococcus infections caused 100,000 – 135,000 hospitalizations due to pneumonia, 6 million cases of otitis media (ear), and 3300 cases of meningitis in the United States. Since the introduction of the conjugate vaccine in 2001, the incidence of sterile infections has decreased from 21-33 cases per 100,000 population to 13 cases per 100,000 population in the United States. Moreover, recurrent otitis can lead to hearing impairment. Fourteen percent of people hospitalized for invasive pneumococcal infection of sterile areas, such as meningitis, result in death. Also, meningitis can lead to learning disabilities and possible neurological sequelae. Elderly, young children (< 2 years old), African-Americans, American Indians, Alaska Natives, children who attend day care centers, and people with medical conditions such as HIV infections or sickle-cell disease are all at high risk for infection. There have been outbreaks in institutional settings and in childcare centers [3].

In the United States the strains resistant to multiple classes of drugs is increasing. Several states in the United States of America have commanded that reporting of drug-resistance Streptococcus pneumoniae and all invasive disease in children, and several states carry out population-based surveillance. Additionally, a system tracks invasive diseases that arise in children (< 5 years old) that have been vaccinated. The number of young children and young adults infected by S. pneumoniae has been decreasing due to better HIV treatment and the implementation of the conjugate vaccine for children [3].



Meningitis can be caused by an invasive pneumococcal infection of the brain and spine. There are many symptoms associated this disease, and the bacterial meningitis caused by Streptococcus pneumoniae can result in severe symptoms. The signs and symptoms of meningitis normally develop 3-7 days post-exposure. The early signs of meningitis can resemble the symptoms influenza. For adults, symptoms can include: fever, distinct and severe headache, stiff neck, nausea, vomiting, photophobia (light sensitivity), lack of interest in eating or drinking, seizures, sleepiness, or an altered mental status (confusion). For infants, symptoms can include: constant crying, excessive sleepiness and irritability, inactivity, poor feeding, high fever, stiffness in the baby’s body or neck, seizures, or a bulge in the soft spot on top of a baby’s head (fontanel). A late symptom of bacterial meningitis can be going into a coma [5,7].

Section 3

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Section 2

Include some current research in each topic, with at least one figure showing data.

Section 3

Include some current research in each topic, with at least one figure showing data.


Overall paper length should be 3,000 words, with at least 3 figures.


[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2011, Kenyon College.