Pneumococcal infection: Wikis


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The most infectionous disease ever

Pneumococcal infection
Classification and external resources
MeSH D011008

Pneumococcal infection refers to an infection caused by Streptococcus pneumoniae.



S. pneumoniae is normally found in the nasopharynx of 5-10% of healthy adults, and 20-40% of healthy children.[1] It can be found in higher amounts in certain environments, especially those where people are spending a great deal of time in close proximity to each other (day care centers, army barracks). It attaches to nasopharyngeal cells through interaction of bacterial surface adhesins. This normal colonization can become infectious if the organisms are carried into areas such as the Eustachian tube or nasal sinuses where it can cause otitis media and sinusitis, respectively. Pneumonia occurs if the organisms are inhaled into the lungs and not cleared (again, viral infection, or smoking-induced ciliary paralysis might be contributing factors). Once the organism makes its way to a site where it is not normally found, it activates the complement protein group, stimulates cytokine production, and attracts white blood cells (specifically neutrophils). The organism's polysaccharide capsule makes it resistant to phagocytosis, and if there is no pre-existing anticapsular antibody, alveolar macrophages cannot adequately kill the pneumococci. The organism spreads to the blood stream (where it can cause bacteremia) and is carried to the meninges, joint spaces, bones, and peritoneal cavity, and may result in meningitis, brain abscess, septic arthritis, or osteomyelitis.

S. pneumoniae has several virulence factors, including the polysaccharide capsule mentioned earlier, that help it evade a host's immune system. It has pneumococcal surface proteins that inhibit complement-mediated opsonization, and it secretes IgA1 protease that will destroy secretory IgA produced by the body and mediates its attachment to respiratory mucosa.

The risk of pneumococcal infection is much increased in persons with impaired IgG synthesis, impaired phagocytosis, or defective clearance of pneumococci. In particular, the absence of a functional spleen, through congenital asplenia, splenectomy, or sickle-cell disease predisposes one to a more severe course of infection (Overwhelming post-splenectomy infection) and prevention measures are indicated (see asplenia).

There is an association between pneumococcal pneumonia and influenza.[2] Damage to the lining of the airways (respiratory epithelium) caused by influenza may facilitate pneumococcal entry and infection.

Virulence Factors

S. pneumoniae expresses different virulence factors on its cell surface and inside the organism. These virulence factors contribute to some of the clinical manifestations during infection with S. pneumoniae.

  • Polysaccharide capsule -prevents phagocytosis by host immune cells by inhibiting C3b opsonization of the bacterial cells
  • Pneumolysin (Ply) -a 53-kDa pore forming protein that can cause lysis of host cells and activate complement
  • Autolysin (LytA) -activation of this protein lyses the bacteria releasing its internal contents (i.e. pneumolysin)
  • Hydrogen peroxide - causes damage to host cells (can cause apoptosis in neuronal cells during meningitis) and has bactericidal effects against competing bacteria (Haemophilus influenzae, Neisseria meningitidis, Staphylococcus aureus)[3][4]
  • Pili - hair-like structures that extend from the surface of many strains of S. pneumoniae. They contribute to colonization of upper respiratory tract and increase the formation of large amounts of TNF by the immune system during sepsis, raising the possibility of septic shock[5]
  • Choline binding protein A/Pneumococcal surface protein A (CbpA/PspA) -an adhesin that can interact with carbohydrates on the cell surface of pulmonary epithelial cells and can inhibit complement-mediated opsonization of pneumococci

Humoral immunity

In the 19th century, it was demonstrated that immunization of rabbits with killed pneumococci protected them against subsequent challenge with viable pneumococci. Serum from immunized rabbits or from humans who had recovered from pneumococcal pneumonia also conferred protection. In the 20th century, the efficacy of immunization was demonstrated in South African miners.

It was discovered that the pneumococcus's capsule made it resistant to phagocytosis, and in the 1920s it was shown that an antibody specific for capsular polysaccharide aided the killing of S. pneumoniae. In 1936, a pneumococcal capsular polysaccharide vaccine was used to abort an epidemic of pneumococcal pneumonia. In the 1940s, experiments on capsular transformation by pneumococci first identified DNA as the material that carries genetic information.

In 1900, it was recognized that different serovars of pneumococci exist, and that immunization with a given serovar did not protect against infection with other serovars. Since then over ninety serovars have been discovered, each with a unique polysaccharide capsule which can be identified by the quellung reaction. Because some of these serovars cause disease more commonly than others, it is possible to provide reasonable protection by immunizing with less than 90 serovars; the current vaccine contains 23 serovars (i.e., it is "23-valent").

The serovars are numbered according to two systems: the American system, which numbers them in the order in which they were discovered, and the Danish system which groups them according to antigenic similarities.


Depending on the nature of infection, an appropriate sample is collected for laboratory identification. Pneumococci are typically gram positive, cocci, seen in pairs or chains. When cultured on blood agar plates with added optochin antibiotic disk, they show alpha-hemolytic colonies and a clear zone of inhibition around the disk meaning they're sensitive to the antibiotic. Pneumococci are also bile soluble. Just like other streptococci, they are catalase negative. A Quellung test can identify specific capsular polysaccharides.[6]

Pneumococcal antigen (cell wall C polysaccharide) may be detected in various body fluids. Older detection kits, based on latex agglutination, added little value above Gram staining and were occasionally false-positive. Better results are achieved with rapid immunochromatography, which has a sensitivity (identifies the cause) of 70-80% and >90% specificity (when positive identifies the actual cause) in pneumococcal infections. The test was initially validated on urine samples, but has been applied successfully to other body fluids.[6]


Historically, treatment relied primarily on β-lactam antibiotics. In the 1960s, nearly all strains of S. pneumoniae were susceptible to penicillin, but since that time, there has been an increasing prevalence of penicillin resistance, especially in areas of high antibiotic use. A varying proportion of strains may also be resistant to cephalosporins, macrolides (such as erythromycin), tetracycline, clindamycin and the quinolones. Penicillin-resistant strains are more likely to be resistant to other antibiotics. Most isolates remain susceptible to vancomycin, though its use in a β-lactam-susceptible isolate is less desirable because of tissue distribution of the drug and concerns of development of vancomycin resistance. More advanced beta-lactam antibiotics (cephalosporins) are commonly used in combination with other drugs to treat meningitis and community-acquired pneumonia. In adults, recently developed fluoroquinolones such as levofloxacin and moxifloxacin are often used to provide empiric coverage for patients with pneumonia, but in parts of the world where these drugs are used to treat tuberculosis, resistance has been described.[7] Susceptibility testing should be routine, with empiric antibiotic treatment guided by resistance patterns in the community in which the organism was acquired, pending the results. There is currently debate as to how relevant the results of susceptibility testing are to clinical outcome.[8][9] There is slight clinical evidence that penicillins may act synergistically with macrolides to improve outcomes.[10]


Vaccines against Streptococcus pneumoniae are available.


  1. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  2. ^ Walter ND, Taylor TH, Shay DK, et al. (2010). "Influenza Circulation and the Burden of Invasive Pneumococcal Pneumonia during a Non‐pandemic Period in the United States". Clin Infect Dis 50: 175–183. doi:10.1086/649208. 
  3. ^ Pericone, Christopher D., Overweg, Karin, Hermans, Peter W. M., Weiser, Jeffrey N. (2000). "Inhibitory and Bactericidal Effects of Hydrogen Peroxide Production by Streptococcus pneumoniae on Other Inhabitants of the Upper Respiratory Tract". Infect Immun 68 (7): 3990–3997. doi:10.1128/IAI.68.7.3990-3997.2000. PMID 10858213. 
  4. ^ Regev-Yochay G, Trzcinski K, Thompson CM, Malley R, Lipsitch M. (2006). "Interference between Streptococcus pneumoniae and Staphylococcus aureus: In vitro hydrogen peroxide-mediated killing by Streptococcus pneumoniae". J Bacteriol 188 (13): 4996–5001. doi:10.1128/JB.00317-06. PMID 16788209. 
  5. ^ Barocchi M, Ries J, Zogaj X, Hemsley C, Albiger B, Kanth A, Dahlberg S, Fernebro J, Moschioni M, Masignani V, Hultenby K, Taddei A, Beiter K, Wartha F, von Euler A, Covacci A, Holden D, Normark S, Rappuoli R, Henriques-Normark B (2006). "A pneumococcal pilus influences virulence and host inflammatory responses". Proc Natl Acad Sci U S A 103 (8): 2857–2862. doi:10.1073/pnas.0511017103. PMID 16481624. 
  6. ^ a b Werno AM, Murdoch DR (March 2008). "Medical microbiology: laboratory diagnosis of invasive pneumococcal disease". Clin. Infect. Dis. 46 (6): 926–32. doi:10.1086/528798. PMID 18260752. 
  7. ^ Von Gottberg, A.; Klugman, K. P.; Cohen, C.; Wolter, N.; De Gouveia, L.; Du Plessis, M.; Mpembe, R.; Quan, V. et al. (2008). "Emergence of levofloxacin-non-susceptible Streptococcus pneumoniae and treatment for multidrug-resistant tuberculosis in children in South Africa: a cohort observational surveillance study". The Lancet 371: 1108. doi:10.1016/S0140-6736(08)60350-5.  edit
  8. ^ Peterson LR (2006). "Penicillins for treatment of pneumococcal pneumonia: does in vitro resistance really matter?". Clin Infect Dis 42 (2): 224–33. doi:10.1086/497594. PMID 16355333. 
  9. ^ Tleyjeh IM, Tlaygeh HM, Hejal R, Montori VM, Baddour LM (2006). "The impact of penicillin resistance on short-term mortality in hospitalized adults with pneumococcal pneumonia: a systematic review and meta-analysis". Clin Infect Dis 42 (6): 788–97. doi:10.1086/500140. PMID 16477555. 
  10. ^ Martínez JA, Horcajada JP, Almela M, et al. (2003). "Addition of a Macrolide to a β-Lactam based empirical antibiotic regimen is associated with lower in-hospital mortality for patients with bacteremic pneumococcal pneumonia". Clin Infect Dis 36: 389–395. doi:10.1086/367541. PMID 12567294. 

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