Mycoplasma pneumoniae

Last updated on: 02.04.2021

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Definition
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Species of the family Mycoplasmataceae in the order Mycoplasmatales. The order Mycoplasmatales belongs to the class of Mollicutes (the soft-skinned), cell-wall-less prokaryotes.

Mycoplasmas (like almost all representatives of the Mollicutes) have no cell wall, murein is not present. Mycoplasmas are the smallest bacteria that can be cultured in cell-free media, measuring 0.3-0.8 μm. Their genome is very small, about 1/5 of E. coli. Mycoplasma pneumoniae is the most important human pathogenic member of the genus Mycoplasma. It does not belong to the normal flora of humans.

Pathogen
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Pathogen characteristics:

  • Small genome size
  • Main lipid body is cholesterol
  • Mycoplasmas do not have the genetic information to produce cholesterol. This must be supplied from the outside
  • Mycoplasmas do not have a rigid cell wall, thus no characteristic shape. They sometimes appear as balls, drops, rings, discs or threads.
  • Mycoplasmas do not have their own nucleotide synthesis
  • Mycoplasmas do not have their own amino acid synthesis
  • Mycoplasmas do not have their own citric acid cycle
  • Mycoplasmas do not produce catalase or peroxidase

Occurrence
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Schoolchildren and young adults are most often affected. Familial accumulations are explained by the high contagiousness and the mode of infection

Etiology
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The germ is transmitted aerogenically by droplet infection, more rarely by smear infection. The contagiousness is very high. Already 100 germs in the target organ lung are sufficient for an infection.

Pathophysiology
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Mycoplasma pneumoniae is an important cause ofcommunity-acquired pneumonia in children and adolescents( Lee H et al. 2018).

Mycoplasma pneumoniae attaches to the ciliated epithelia of the bronchial system via neuraminic acid receptors. Production of H2O2 and other toxins destroys the cells. Mycoplasmas produce superantigens, which not only stimulate antigen-specific T lymphocytes to produce cytokines. Furthermore, various antigens cross-react with the body's own antigens. Furthermore, various antigens cross-react with the body's own molecular structures, which results in autoimmune phenomena. Thus, cold agglutinins are frequently detected.

Clinical picture
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incubation period of about 3 weeks. Thensymptoms of severe colds with pharyngitis or tracheobronchitis. Cough is a dominant phenomenon. In 5-25% development of atypical pneumonia. Frequent formation of cold agglutinins during the acute phase of infection.

Diagnostics
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Culture is time-consuming and is not routinely performed. The test material is nasopharyngeal secretion or a swab from the throat (caution: dehydration).

Direct detection by DNA hybridisation or PCR

Serological detection of antibodies (ELISA technique)

Differential diagnosis
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Virus-induced pneumonia, Q fever

Complication(s)
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Lower respiratory tract infections with M. pneumoniae are not infrequently associated with exacerbations of asthma in children (Kumar S et al. 2019). Bar Meir E et al described " thrombotic thrombocytopenic purpura (Moschcowitz syndrome). Furthermore, formation of cryoglobulins may occur during the acute phase of infection. A connection between M. pneumoniae infections and Tourette's syndrome is being discussed (Müller N et al. 2004).

Therapy
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Treatment with antibiotics may not be necessary in mild cases due to the self-healing nature of M. pneumoniae infection (Lee H et al. 2018).

When clinical symptoms are appropriate, macrolides are recommended as first-line therapy, but macrolide resistance rates have increased significantly in pediatric M. pneumoniae (Tanaka T et al. 2017).

In contrast, antibiotic treatment of severe cases of M. pneumoniae pneumonia is complicated. The clinical benefit of tetracyclines and fluoroquinolones has been shown in some reports in terms of shortening symptom duration and rapid resolution (Lee H et al. 2018).

Prognose
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generally good prognosis.

Literature
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  1. Atkinson TP et al (2008) Epidemiology, clinical manifestations, pathogenesis and laboratory detection of Mycoplasma pneumoniae infections. FEMS Microbiol Rev 32:956-973.
  2. Bar Meir E et al (2000) Mycoplasma pneumoniae-induced thrombotic thrombocytopenic purpura. Acta Haematol 103:112-115.
  3. Hammerschlag MR (2001) Mycoplasma pneumoniae infections. Curr Opin Infect Dis 14:181-186.
  4. Kumar S (2018) Mycoplasma pneumoniae: A significant but underrated pathogen in paediatric community-acquired lower respiratory tract infections. Indian JMed Res 147:23-31.
  5. Kumar S et al (2019) Mycoplasma pneumoniae infection and asthma in children. Trop Doct 49:117-119.
  6. Lee H et al (2018) Antimicrobial therapy of macrolide-resistant Mycoplasma pneumoniae pneumonia in children. Expert Rev Anti Infect Ther 16:23-34.
  7. Medjo B et al. (2014) Mycoplasma pneumoniae as a causative agent of community-acquired pneumonia in children: clinical features and laboratory diagnosis. Ital J Pediatr 40:104.
  8. Müller N et al (2004) Mycoplasma pneumoniae infection and Tourette's syndrome. Psychiatry Res 129:119-125.
  9. Tanaka T et al (2017) Macrolide-resistant Mycoplasma pneumoniae infection, Japan, 2008-2015. Emerg Infect Dis 23:1703-1706.

Last updated on: 02.04.2021