| Mycoplasma pneumonia | |
|---|---|
| Specialty | Infectious disease,pulmonology |
| Complications | Stevens–Johnson syndrome,autoimmune hemolytic anemia, cardiovascular diseases,encephalitis,Guillain–Barré syndrome[citation needed] |
Mycoplasma pneumonia is a form ofbacterial pneumonia caused by the bacteriumMycoplasma pneumoniae.
M. pneumoniae is known to cause a host of symptoms such asprimary atypical pneumonia,tracheobronchitis, andupper 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 requirehospitalization.[1] Common mild symptoms includesore throat,wheezing andcoughing,fever,headache,rhinitis,myalgia andfeelings of unease, in which symptom intensity and duration can be limited by early treatment withantibiotics. Rarely,M. pneumoniae pneumonia results in death due tolesions andulceration of the epithelial lining,pulmonary edema, andbronchiolitis obliterans.
Non-pulmonary symptoms such as autoimmune responses,central nervous system complications, anddermatological disorders have been associated withM. pneumoniae infections in up to 25% of cases.[1] Hemolysis occurs regularly, but often remains asymptomatic (fatigue, Raynaud syndrome only in cold season), as well as carditis, joint disease, and gastrointestinal disease.
Mycoplasma pneumoniae is spread throughrespiratory droplet andaerosol transmission.[3]
Once attached to the mucosa of a host organism,M. pneumoniae extracts nutrients, grows, and reproduces bybinary fission. Attachment sites include the upper and lower respiratory tract, causingpharyngitis,bronchitis, andpneumonia. The infection caused by this bacterium is calledatypical pneumonia because of its protracted course and lack ofsputum production and wealth of non-pulmonary symptoms. ChronicMycoplasma infections have been implicated in the pathogenesis ofrheumatoid arthritis and other rheumatological diseases.[citation needed]
Mycoplasma atypical pneumonia can be complicated byStevens–Johnson syndrome,autoimmune hemolytic anemia, cardiovascular diseases,encephalitis, orGuillain–Barré syndrome.[citation needed]
Diagnosis ofMycoplasma 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 forM. pneumoniae.[1]
Historically, the diagnosis ofM. pneumoniae infections was made based on the presence ofcold agglutinins (though this method should be used cautiously due to its mediocre and poorsensitivity and specificity, respectively). Additionally, the ability of the infected material to reducetetrazolium was also considered. While laboratory testing is crucial for causative diagnosis, these methods are more practical for epidemiological studies than for patient diagnosis.[1]Culture tests are rarely used as diagnostic tools; ratherimmunoblotting,immunofluorescent staining, hemadsorption tests, tetrazolium reduction,metabolic inhibition tests,serological assays, andpolymerase chain reaction (PCR) are used for diagnosis and characterization ofbacterial pneumonic infections.[1] PCR is the most rapid and effective way to determine the presence ofM. pneumoniae, however the procedure does not indicate the activity orviability of the cells present.[2][4]Enzyme immunoassay (EIA) serological assays are the most common method ofM. 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 diagnoseM. pneumoniae infections.[citation needed]
While antibiotics with activity specifically againstM. pneumoniae are often used (e.g.,erythromycin ordoxycycline), 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.[5]
The majority of antibiotics used to treatM. pneumoniae infections are targeted at bacterialrRNA inribosomal complexes, includingmacrolides,tetracycline,ketolides, andfluoroquinolone, many of which can be administered orally.[1][6] Macrolides are capable of reducing hyperresponsiveness and protecting the epithelial lining fromoxidative and structural damage, however they are capable only of inhibiting bacteria (bacteriostatic) and are not able to cause bacterial cell death.[1][7] The most common macrolides used in the treatment of infected children in Japan are erythromycin andclarithromycin, which inhibit bacterial protein synthesis by binding23S rRNA.[6] Administration of antibiotics has been proven to reduce the longevity and intensity ofM. pneumoniae infections in comparison to cases left untreated. Additionally, some high-dose steroid therapies have shown to reverseneurological effects in children with complicated infections.[1]
The difficulty in eradicatingMycoplasma pneumoniae infections is due to the ability of the bacterium to persist within an individual, as well as the lack of cell wall inM. pneumoniae, which renders multiple antibiotics directed at the bacterial cell wall ineffective in treating infections.[1]M. pneumoniae therefore displays resistance to antimicrobials such asβ-lactams,glycopeptides,sulfonamides,trimethoprim,polymixins,nalidixic acid, andrifampin.[1][2] Antimicrobial drug resistance rates forM. pneumoniae were determined in clinical specimens and isolates obtained during 2011–2012 in Ontario, Canada. Of 91M. pneumoniae drug-resistant specimens, 11 (12.1%) carried nucleotide mutations associated withmacrolide resistance in the23S rRNA gene. None of theM. pneumoniae specimens were resistant tofluoroquinolones ortetracyclines.[8]
Transmission ofMycoplasma pneumoniae infections is difficult to limit because of the several day period of infection before symptoms appear.[9] The lack of proper diagnostic tools and effective treatment for the bacterium also contribute to the outbreak of infection.[9] Usingnetwork theory, Meyerset al. analyzed the transmission ofM. pneumoniae infections and developed control strategies based on the created model. They determined thatcohorting patients is less effective due to the longincubation period, and so the best method of prevention is to limitcaregiver–patient interactions and reduce the movement of caregivers to multiplehospital wards.[10]
As with all airborne disease,airborne precautions and routine indoor air management tools are likely to reduce transmission.
Vaccine design forM. pneumoniae has been focused primarily on prevention of host cell attachment, which would prevent initiation ofcytotoxicity 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 systemsensitization.[1] Recent experiments in mouse models have linked this phenomenon to immune system sensitization by the lipid moieties ofM. pneumoniae lipoproteins.[11] Introduction ofpeptides that block adhesion receptors on the surface of the host cell may also be able to prevent attachment ofM. pneumoniae.[12]
The prevalence of mycoplasma pneumonia (MP) is greater among children than adults.[13][3][14] Many adults remain asymptomatic, while children typically do not.[3]
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 respiratorypathogens are less prevalent. Reinfection andepidemic cycling is thought to be a result of P1 adhesin subtype variation.[1] Approximately 40% of community-acquiredpneumonia is due toM. pneumoniae infections, with children and elderly individuals being mostsusceptible, however no personal risk factors for acquiringM. pneumoniae induced pneumonia have been determined.[1][2] Transmission ofM. pneumoniae can only occur through close contact and exchange ofaerosols by coughing due to the increased susceptibility of thecell wall-lacking organism todesiccation.Outbreaks ofM. pneumoniae infections tend to occur within groups of people in close and prolonged proximity, including schools, institutions, military bases, andhouseholds.[1]
Rates ofMycoplasma pneumonia in all globalcommunity-acquired pneumonia (CAP) cases range from 10-15%.[13][14] The rate ofMycoplasma pneumonia in adults with CAP is estimated to be 15%, and the rate of in children with CAP has been reported at 27.4%.[3] The rates ofM. pneumoniae among hospitalized CAP cases are 35% in adults[14] and 24% in children.[3] Rates of hospitalizations among adults increase with age.[3]M. pneumoniae has been shown to act as a trigger for other lung diseases.[14]
Cases ofM. pneumoniae may be unreported due to patients with few or no symptoms not seeking medical care.[13][14] On a global scale, differences in lab techniques and sampling methods can also impact the reported number of cases.[13]
M. pneumoniae can be spread by droplets and aerosols, typically from an infected person coughing or sneezing.[3] 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.[13][3][14] It is thought that factors such as climate, season, and geography have little impact on rates ofM. pneumoniae.[3] 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.[3][14] It is thought that weather events likeEl Niño can impact the yearly cycles and seasonal difference between continents.[14]
