A Compendium for Mycoplasma pneumoniae

Abstract

Historically, atypical pneumonia was a term used to describe an unusual presentation of pneumonia. Currently, it is used to describe the multitude of symptoms juxtaposing the classic symptoms found in cases of pneumococcal pneumonia. Specifically, atypical pneumonia is a syndrome resulting from a relatively common group of pathogens including Chlamydophila sp., and Mycoplasma pneumoniae. The incidence of M. pneumoniae pneumonia in adults is less than the burden experienced by children. Transmission rates among families indicate children may act as a reservoir and maintain contagiousness over a long period of time ranging from months to years. In adults, M. pneumoniae typically produces a mild, "walking" pneumonia and is considered to be one of the causes of persistent cough in patients. M. pneumoniae has also been shown to trigger the exacerbation of other lung diseases. It has been repeatedly detected in patients with bronchitis, asthma, chronic obstructive pulmonary disorder, and cystic fibrosis. Recent advances in technology allow for the rapid diagnosis of M. pneumoniae through the use of polymerase chain reaction or rapid antigen tests. With this, more effort has been afforded to identify the causative etiologic agent in all cases of pneumonia. However, previous practices, including the overprescribing of macrolide treatment in China and Japan, have created increased incidence of macrolide-resistant M. pneumoniae. Reports from these countries indicate that >85% of M. pneumoniae pneumonia pediatric cases are macrolide-resistant. Despite its extensively studied past, the smallest bacterial species still inspires some of the largest questions. The developments in microbiology, diagnostic features and techniques, epidemiology, treatment and vaccines, and upper respiratory conditions associated with M. pneumoniae in adult populations are included within this review.

Acute respiratory distress syndrome related to Mycoplasma pneumoniae infection

“…This indeed does not allow firmly establishing the diagnosis of M. pneumoniae infection when the diagnosis relies on paired antibody titers that require several weeks to show seroconversion. Our case as other recent reports suggest that rapid, accurate, and readily available diagnostic test such as multiplex PCR assay for detection of five pneumonia-causing bacteria may improve detection of M. pneumoniae in ARDS patients [10], [11].…”

Relationships between Th1/Th2 cytokine profiles and chest radiographic manifestations in childhood<em> Mycoplasma pneumoniae</em> pneumonia

“…However, many cases develop into lower respiratory tract infections or even severe pneumonia. MP is one of the most common causes of CAP in children and can cause serious and life-threatening pulmonary and extrapulmonary complications 6. Over the past few years, macrolide-resistant MP (MRMP) has been reported in the literature, particularly in some Asian countries.…”

“…The incidence of Mycoplasma pneumoniae pneumonia (MPP) has been increasing in recent years. MPP can lead to many kinds of pulmonary complications, including pleural effusion, asthma, chronic interstitial fibrosis, and acute respiratory distress syndrome 5,6. However, the pathogenesis of MPP is not completely clear.…”

Cambiando los paradigmas de la infección por M. pneumoniae en pediatría

“…45 La denominada toxina CARDS (acrónimo por sus siglas en inglés de Community Acquired Respiratory Distress Syndrome) es una toxina vacuolizante y ribosilante de ADP; presenta homología con la subunidad S1 de la toxina pertussis, la cual tiene una alta afinidad al surfactante-A a nivel alveolar. 46 En modelos animales induce una respuesta proinflamatoria en el tracto respiratorio, estimula la producción de IL-1, IL-6, IL-12 y TNF-α e incrementa la expresión de la respuesta inflamatoria vía Th2, con producción predominante de las citoquinas IL-4, IL-3 y de las quimoquinas CCL-7 y CCL-32. También la toxina CARDS produce inflamación a través de la regulación del inflamosoma, que es un complejo multiprotéico localizado a nivel citoplasmático y es el responsable de la activación de la enzima caspasa-1, la cual a su vez activa el paso de pro-IL-1b a IL-1b.…”

“…También la toxina CARDS produce inflamación a través de la regulación del inflamosoma, que es un complejo multiprotéico localizado a nivel citoplasmático y es el responsable de la activación de la enzima caspasa-1, la cual a su vez activa el paso de pro-IL-1b a IL-1b. 42,46 También se han reconocido más de 30 lipoproteínas de M. pneumoniae que poseen potentes propiedades inflamatorias, como son la N-ALP1/N-ALP2 y la F0F1-ATPasa, que también activan el NF-kb, vía TLR-1, TLR-2 y TLR-6, que ocasionan movilización y reclutamiento de linfocitos y neutrófilos a nivel pulmonar, produciendo inflamación. 45 Desde el punto de vista histopatológico hay ulceración y descamación de la mucosa respiratoria, con destrucción del epitelio ciliado.…”