Mycoplasma pneumonia

Template:Infobox medical condition (new) Mycoplasma pneumonia is a form of bacterial pneumonia caused by the bacterium Mycoplasma pneumoniae.

Signs and symptoms

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.<ref name="Waites">Template:Cite journal</ref><ref name="Daxboeck">Template:Cite journal</ref> 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.<ref name="Waites" /> 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.

Non-pulmonary 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.<ref name="Waites" /> Hemolysis occurs regularly, but often remains asymptomatic (fatigue, Raynaud syndrome only in cold season), as well as carditis, joint disease, and gastrointestinal disease.

Cause

Mycoplasma pneumoniae is spread through respiratory droplet and aerosol transmission.<ref name="Kashyap-2010" />

Pathophysiology

Template:See also 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 non-pulmonary symptoms. Chronic Mycoplasma infections have been implicated in the pathogenesis of rheumatoid arthritis and other rheumatological diseases.Template:Cn

Mycoplasma atypical pneumonia can be complicated by Stevens–Johnson syndrome, autoimmune hemolytic anemia, cardiovascular diseases, encephalitis, or Guillain–Barré syndrome.Template:Cn

Diagnosis

Diagnosis of Mycoplasma pneumoniae infections is complicated by its associated 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.<ref name="Waites" />

Historically, the diagnosis of M. pneumoniae infections was made based on the presence of cold agglutinins (though this method should be used cautiously due to its mediocre and poor sensitivity and specificity, respectively). Additionally, the ability of the infected material to reduce tetrazolium was also considered. While laboratory testing is crucial for causative diagnosis, these methods are more practical for epidemiological studies than for patient diagnosis.<ref name="Waites" /> 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.<ref name="Waites" /> 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.<ref name="Daxboeck" /><ref name="pmid9774556">Template:Cite journal</ref> 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.<ref name="Waites" /> 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.Template:Citation needed

Treatment

While antibiotics with activity specifically against M. pneumoniae are often used (e.g., erythromycin or 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.<ref>Template:Cite journal</ref>

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.<ref name="Waites" /><ref name="Matsuoka">Template:Cite journal</ref> 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.<ref name="Waites" /><ref name="Dallo">Template:Cite journal</ref> 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.<ref name="Matsuoka" /> 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.<ref name="Waites" />

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.<ref name="Waites" /> M. pneumoniae therefore displays resistance to antimicrobials such as β-lactams, glycopeptides, sulfonamides, trimethoprim, polymixins, nalidixic acid, and rifampin.<ref name="Waites" /><ref name="Daxboeck" /> Antimicrobial drug resistance rates for M. 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.<ref>Template:Cite journal</ref>

Prevention

Transmission of Mycoplasma pneumoniae infections is difficult to limit because of the several day period of infection before symptoms appear.<ref name="Meyers">Template:Cite journal</ref> The lack of proper diagnostic tools and effective treatment for the bacterium also contribute to the outbreak of infection.<ref name="Meyers" /> 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 hospital wards.<ref name="Meyers2">Template:Cite journal</ref>

As with all airborne disease, airborne precautions and routine indoor air management tools are likely to reduce transmission.

Vaccine design for M. pneumoniae has been focused primarily on prevention of host cell attachment, which would prevent initiation of cytotoxicity and subsequent symptoms.<ref name="Waites" /> 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.<ref name="Waites" /> Recent experiments in mouse models have linked this phenomenon to immune system sensitization by the lipid moieties of M. pneumoniae lipoproteins.<ref>Template:Cite journal</ref> Introduction of peptides that block adhesion receptors on the surface of the host cell may also be able to prevent attachment of M. pneumoniae.<ref name="Drasbek">Template:Cite journal</ref>

Epidemiology

The prevalence of mycoplasma pneumonia (MP) is greater among children than adults.<ref name="Marchello-2016">Template:Cite journal</ref><ref name="Kashyap-2010">Template:Cite journal</ref><ref name="Parrott-2016">Template:Cite journal</ref> Many adults remain asymptomatic, while children typically do not.<ref name="Kashyap-2010" />

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.<ref name="Waites" /> 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.<ref name="Waites" /><ref name="Daxboeck" /> 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.<ref name="Waites" />

Rates of Mycoplasma pneumonia in all global community-acquired pneumonia (CAP) cases range from 10-15%.<ref name="Marchello-2016" /><ref name="Parrott-2016" /> 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%.<ref name="Kashyap-2010" /> The rates of M. pneumoniae among hospitalized CAP cases are 35% in adults<ref name="Parrott-2016" /> and 24% in children.<ref name="Kashyap-2010" /> Rates of hospitalizations among adults increase with age.<ref name="Kashyap-2010" /> M. pneumoniae has been shown to act as a trigger for other lung diseases.<ref name="Parrott-2016" />

Cases of M. pneumoniae may be unreported due to patients with few or no symptoms not seeking medical care.<ref name="Marchello-2016" /><ref name="Parrott-2016" /> On a global scale, differences in lab techniques and sampling methods can also impact the reported number of cases.<ref name="Marchello-2016" />

M. pneumoniae can be spread by droplets and aerosols, typically from an infected person coughing or sneezing.<ref name="Kashyap-2010" /> If a person still has a cough, they can remain infectious even after a majority of other symptoms disappear.<ref name="Parrott-2016" />

Outbreaks follow a 3–7 year cycle.<ref name="Marchello-2016" /><ref name="Kashyap-2010" /><ref name="Parrott-2016" /> It is thought that factors such as climate, season, and geography have little impact on rates of M. pneumoniae.<ref name="Kashyap-2010" /> 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.<ref name="Kashyap-2010" /><ref name="Parrott-2016" /> It is thought that weather events like El Niño can impact the yearly cycles and seasonal difference between continents.<ref name="Parrott-2016" />

See also

• Mycoplasmal pneumonia of swine