Mycoplasma pneumonia

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Mycoplasma pneumonia
SpecialtyInfectious disease, pulmonology
ComplicationsStevens–Johnson syndrome, autoimmune hemolytic anemia, cardiovascular diseases, encephalitis, Guillain–Barré syndrome[citation needed]

Mycoplasma pneumonia is a form of bacterial pneumonia caused by the bacterium Mycoplasma pneumoniae.

Signs and symptoms[edit]

M. pneumoniae is known to cause a host of symptoms such as primary atypical pneumonia, tracheobronchitis, and upper respiratory tract disease. Primary atypical pneumonia is one of the most severe types of manifestation, with tracheobronchitis being the most common symptom and another 15% of cases, usually adults, remain asymptomatic.[1][2] Symptomatic infections tend to develop over a period of several days and manifestation of pneumonia can be confused with a number of other bacterial pathogens and conditions that cause pneumonia. Tracheobronchitis is most common in children due to a reduced immune system capacity, and up to 18% of infected children require hospitalization.[1] Common mild symptoms include sore throat, wheezing and coughing, fever, headache, rhinitis, myalgia and feelings of unease, in which symptom intensity and duration can be limited by early treatment with antibiotics. Rarely, M. pneumoniae pneumonia results in death due to lesions and ulceration of the epithelial lining, pulmonary edema, and bronchiolitis obliterans. Extrapulmonary symptoms such as autoimmune responses, central nervous system complications, and dermatological disorders have been associated with M. pneumoniae infections in up to 25% of cases.[1]


Mycoplasma pneumoniae is spread through respiratory droplet transmission.[citation needed]


Once attached to the mucosa of a host organism, M. pneumoniae extracts nutrients, grows, and reproduces by binary fission. Attachment sites include the upper and lower respiratory tract, causing pharyngitis, bronchitis, and pneumonia. The infection caused by this bacterium is called atypical pneumonia because of its protracted course and lack of sputum production and wealth of extrapulmonary symptoms. Chronic Mycoplasma infections have been implicated in the pathogenesis of rheumatoid arthritis and other rheumatological diseases.[citation needed]

Mycoplasma atypical pneumonia can be complicated by Stevens–Johnson syndrome, autoimmune hemolytic anemia, cardiovascular diseases, encephalitis, or Guillain–Barré syndrome.[citation needed]


Diagnosis of Mycoplasma pneumoniae infections is complicated by the delayed onset of symptoms and the similarity of symptoms to other pulmonary conditions. Often, M. pneumoniae infections are diagnosed as other conditions and, occasionally, non-pathogenic mycoplasmas present in the respiratory tract are mistaken for M. pneumoniae.[1]

Historically, diagnosis of M. pneumoniae infections was made based on the presence of cold agglutinins (should be used with caution due to mediocre sensitivity and poor specificity) and the ability of the infected material to reduce tetrazolium. Causative diagnosis is dependent upon laboratory testing, however these methods are more practical in epidemiological studies than in patient diagnosis.[1] Culture tests are rarely used as diagnostic tools; rather immunoblotting, immunofluorescent staining, hemadsorption tests, tetrazolium reduction, metabolic inhibition tests, serological assays, and polymerase chain reaction (PCR) are used for diagnosis and characterization of bacterial pneumonic infections.[1] PCR is the most rapid and effective way to determine the presence of M. pneumoniae, however the procedure does not indicate the activity or viability of the cells present.[2][3] Enzyme immunoassay (EIA) serological assays are the most common method of M. pneumoniae detection used in patient diagnosis due to the low cost and relatively short testing time. One drawback of serology is that viable organisms are required, which may overstate the severity of infection.[1] Neither of these methods, along with others, has been available to medical professionals in a rapid, efficient and inexpensive enough form to be used in routine diagnosis, leading to decreased ability of physicians to diagnose M. pneumoniae infections.[citation needed]


While antibiotics with activity specifically against M. pneumoniae are often used (e.g., erythromycin, doxycycline), it is unclear if these result in greater benefit than using antibiotics without specific activity against this organism in those with an infection acquired in the community.[4]

The majority of antibiotics used to treat M. pneumoniae infections are targeted at bacterial rRNA in ribosomal complexes, including macrolides, tetracycline, ketolides, and fluoroquinolone, many of which can be administered orally.[1][5] Macrolides are capable of reducing hyperresponsiveness and protecting the epithelial lining from oxidative and structural damage, however they are capable only of inhibiting bacteria (bacteriostatic) and are not able to cause bacterial cell death.[1][6] The most common macrolides used in the treatment of infected children in Japan are erythromycin and clarithromycin, which inhibit bacterial protein synthesis by binding 23S rRNA.[5] Administration of antibiotics has been proven to reduce the longevity and intensity of M. pneumoniae infections in comparison to cases left untreated. Additionally, some high-dose steroid therapies have shown to reverse neurological effects in children with complicated infections.[1]

The difficulty in eradicating Mycoplasma pneumoniae infections is due to the ability of the bacterium to persist within an individual, as well as the lack of cell wall in M. pneumoniae, which renders multiple antibiotics directed at the bacterial cell wall ineffective in treating infections.[1] M. pneumoniae therefore displays resistance to antimicrobials such as β-lactams, glycopeptides, sulfonamides, trimethoprim, polymixins, nalidixic acid, and rifampin.[1][2] Antimicrobial drug resistance rates for Mycoplasma pneumoniae were determined in clinical specimens and isolates obtained during 2011–2012 in Ontario, Canada. Of 91 M. pneumoniae drug-resistant specimens, 11 (12.1%) carried nucleotide mutations associated with macrolide resistance in the 23S rRNA gene. None of the M. pneumoniae specimens were resistant to fluoroquinolones or tetracyclines.[7]



Transmission of Mycoplasma pneumoniae infections is difficult to limit because of the several day period of infection before symptoms appear.[8] The lack of proper diagnostic tools and effective treatment for the bacterium also contribute to the outbreak of infection.[8] Using network theory, Meyers et al. analyzed the transmission of M. pneumoniae infections and developed control strategies based on the created model. They determined that cohorting patients is less effective due to the long incubation period, and so the best method of prevention is to limit caregiver-patient interactions and reduce the movement of caregivers to multiple wards.[9]

Vaccine design for M. pneumoniae has been focused primarily on prevention of host cell attachment, which would prevent initiation of cytotoxicity and subsequent symptoms.[1] To date, vaccines targeted at the P1 adhesin have shown no reduction in the onset of infection, and some vaccine trials resulted in worsened symptoms due to immune system sensitization.[1] Recent experiments in mouse models have linked this phenomenon to immune system sensitization by the lipid moieties of M. pneumoniae lipoproteins.[10] Introduction of peptides that block adhesion receptors on the surface of the host cell may also be able to prevent attachment of M. pneumoniae.[11]


The prevalence of mycoplasma pneumonia (MP) is greater among children than adults.[12][13][14] Many adults remain asymptomatic, while children typically do not.[13]

The incidence of disease does not appear to be related to season or geography; however, infection tends to occur more frequently during the summer and fall months when other respiratory pathogens are less prevalent. Reinfection and epidemic cycling is thought to be a result of P1 adhesin subtype variation.[1] Approximately 40% of community-acquired pneumonia is due to M. pneumoniae infections, with children and elderly individuals being most susceptible, however no personal risk factors for acquiring M. pneumoniae induced pneumonia have been determined.[1][2] Transmission of M. pneumoniae can only occur through close contact and exchange of aerosols by coughing due to the increased susceptibility of the cell wall-lacking organism to desiccation. Outbreaks of M. pneumoniae infections tend to occur within groups of people in close and prolonged proximity, including schools, institutions, military bases, and households.[1]

Rates of mycoplasma pneumonia in all global community-acquired pneumonia (CAP) cases range from 10-15%.[12][14] The rate of mycoplasma pneumonia in adults with CAP is estimated to be 15%, and the rate of in children with CAP has been reported at 27.4%.[13] The rates of M. pneumonia among hospitalized CAP cases are 35% in adults[14] and 24% in children.[13] Rates of hospitalizations among adults increase with age.[13] M. pneumonia has been shown to act as a trigger for other lung diseases.[14]

Cases of M. pneumonia may be unreported due to patients with little or no symptoms not seeking medical care.[12][14] On a global scale, differences in lab techniques and sampling methods can also impact the reported number of cases.[12]

M. pneumonia can be spread by droplets and aerosols, typically from an infected person coughing or sneezing.[13] If a person still has a cough, they can remain infectious even after a majority of other symptoms disappear.[14]

Outbreaks follow a 3-7 year cycle.[12][13][14] It is thought that factors such as climate, season, and geography have little impact on rates of M. pneumonia.[13] Cases in the United States are more prevalent in the late summer and early fall, while other regions report that seasons did not affect case rate.[13][14] It is thought that weather events like El Niño can impact the yearly cycles and seasonal difference between continents.[14]

See also[edit]


  1. ^ a b c d e f g h i j k l m n o p q Waites KB, Talkington DF (October 2004). "Mycoplasma pneumoniae and its role as a human pathogen". Clinical Microbiology Reviews. 17 (4): 697–728. doi:10.1128/CMR.17.4.697-728.2004. PMC 523564. PMID 15489344.
  2. ^ a b c d Daxboeck F, Krause R, Wenisch C (April 2003). "Laboratory diagnosis of Mycoplasma pneumoniae infection". Clinical Microbiology and Infection. 9 (4): 263–73. doi:10.1046/j.1469-0691.2003.00590.x. PMID 12667235.
  3. ^ Waris ME, Toikka P, Saarinen T, et al. (November 1998). "Diagnosis of Mycoplasma pneumoniae pneumonia in children". J. Clin. Microbiol. 36 (11): 3155–9. doi:10.1128/JCM.36.11.3155-3159.1998. PMC 105292. PMID 9774556.
  4. ^ Biondi, E; McCulloh, R; Alverson, B; Klein, A; Dixon, A (Jun 2014). "Treatment of mycoplasma pneumonia: a systematic review". Pediatrics. 133 (6): 1081–90. doi:10.1542/peds.2013-3729. PMID 24864174.
  5. ^ a b Matsuoka M, Narita M, Okazaki N, Ohya H, Yamazaki T, Ouchi K, et al. (December 2004). "Characterization and molecular analysis of macrolide-resistant Mycoplasma pneumoniae clinical isolates obtained in Japan". Antimicrobial Agents and Chemotherapy. 48 (12): 4624–30. doi:10.1128/AAC.48.12.4624-4630.2004. PMC 529214. PMID 15561835.
  6. ^ Dallo SF, Baseman JB (November 2000). "Intracellular DNA replication and long-term survival of pathogenic mycoplasmas". Microbial Pathogenesis. 29 (5): 301–9. doi:10.1006/mpat.2000.0395. PMID 11031124.
  7. ^ Eshaghi A, Memari N, Tang P, Olsha R, Farrell DJ, Low DE, et al. (2013). "Macrolide-resistant Mycoplasma pneumoniae in humans, Ontario, Canada, 2010-2011". Emerging Infectious Diseases. 19 (9): 1525–1527. doi:10.3201/eid1909.121466. PMC 3810904. PMID 23968896.
  8. ^ a b Ancel Meyers L, Newman ME, Martin M, Schrag S (February 2003). "Applying network theory to epidemics: control measures for Mycoplasma pneumoniae outbreaks". Emerging Infectious Diseases. 9 (2): 204–10. doi:10.3201/eid0902.020188. PMC 3369603. PMID 12603991.
  9. ^ Ancel Meyers L, Newman ME, Martin M, Schrag S (February 2003). "Applying network theory to epidemics: control measures for Mycoplasma pneumoniae outbreaks". Emerging Infectious Diseases. 9 (2): 204–10. doi:10.3201/eid0902.020188. PMC 3369603. PMID 12603991.
  10. ^ Mara AB, Gavitt TD, Tulman ER, Geary SJ, Szczepanek SM (2020-04-08). "Mycoplasma pneumoniae lipoproteins are the causative factor of vaccine-enhanced disease". npj Vaccines. 5 (1): 31. doi:10.1038/s41541-020-0181-x. PMC 7142147. PMID 32284882.
  11. ^ Drasbek M, Christiansen G, Drasbek KR, Holm A, Birkelund S (November 2007). "Interaction between the P1 protein of Mycoplasma pneumoniae and receptors on HEp-2 cells". Microbiology. 153 (Pt 11): 3791–3799. doi:10.1099/mic.0.2007/010736-0. PMID 17975088.
  12. ^ a b c d e Marchello, C.; Dale, A. P.; Thai, T. N.; Han, D. S.; Ebell, M. H. (2016-11-01). "Prevalence of Atypical Pathogens in Patients With Cough and Community-Acquired Pneumonia: A Meta-Analysis". The Annals of Family Medicine. 14 (6): 552–566. doi:10.1370/afm.1993. ISSN 1544-1709. PMC 5389400. PMID 28376442.
  13. ^ a b c d e f g h i Kashyap, Surender; Sarkar, Malay (2010). "Mycoplasma pneumonia: Clinical features and management". Lung India. 27 (2): 75–85. doi:10.4103/0970-2113.63611. ISSN 0970-2113. PMC 2893430. PMID 20616940.
  14. ^ a b c d e f g h i Parrott, Gretchen L.; Kinjo, Takeshi; Fujita, Jiro (2016-04-12). "A Compendium for Mycoplasma pneumoniae". Frontiers in Microbiology. 7: 513. doi:10.3389/fmicb.2016.00513. ISSN 1664-302X. PMC 4828434. PMID 27148202.

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