Mycoplasma pneumoniae is an important cause of upper and lower respiratory tract infections in children as well as adults that can range in severity from mild to life-threatening. For full access to this pdf, sign in to an existing account, or purchase an annual subscription. You will be subject to the destination website's privacy policy when you follow the link. [ 1] M pneumoniae was first isolated in cattle with. M. pneumoniae produces a unique virulence factor known as Community Acquired Respiratory Distress Syndrome (CARDS) toxin. Mycoplasma genitalium is increasingly appreciated as a common cause of sexually transmitted disease syndromes, including urethritis in men and cervicitis, endometritis, pelvic inflammatory disease, and possibly preterm birth, tubal factor infertility, and ectopic pregnancy in women. CDC is not responsible for Section 508 compliance (accessibility) on other federal or private website. In addition, using PCR, these investigators detected the A-to-G mutation in 23 of 94 (24%) PCR-positive oral samples taken from children with respiratory infections. Because the organism is very rarely isolated from clinical specimens, and performance of in vitro susceptibility tests is an even less common procedure, whether naturally occurring resistance to antimicrobial agents occurs to any significant extent is virtually unknown in most countries. A model of cellular activation has been developed in which adherence by the bacterium to surface sialoglycoproteins results in cellular activation through the normal receptor-signaling mechanisms. Mycoplasma pneumoniae is the most common pathogenic species infecting humans. It has been known for many years that persons with mycoplasmal respiratory infections may continue to shed the organisms for following clinical resolution of the illness and antimicrobial therapy (Smith et al., 1967) and that erythromycin-resistant strains can occur and are sometimes isolates from patients who have received prior macrolide therapy (Niitu et al., 1970; Stopler et al., 1980; Stopler & Branski, 1986). Beyond its ability to cause severe lower respiratory illness and milder upper respiratory symptoms it has become apparent that a wide array of extrapulmonary infectious and postinfectious events may accompany the infections in humans caused by this organism. Mycoplasma pneumoniae also directly activates and induces cytokine production from unsorted peripheral blood leukocytes (Kita et al., 1992), lymphocytes (Arai et al., 1983; Simecka et al., 1993), respiratory epithelial cells (Yang et al., 2002; Dakhama et al., 2003; Kraft et al., 2008), and monocyte/macrophages (Yang et al., 2003; Broaders et al., 2006). Although this strain has normal attachment organelle morphology and normal adherence characteristics with respect to red blood cells and cultured alveolar epithelial cells, its ability to interact productively with human bronchial epithelial cells and colonize them is profoundly reduced. Chest radiographs may reveal bibasilar streaky infiltrates. M. pneumoniaeis primarily an extracellular pathogen that has evolved a specialized attachment organelle for close association with host cells. These findings may reflect the greater number of young children who attend day care centers on a regular basis than in previous years, and the ease with which young children share respiratory secretions with older household members or contacts. As would be expected, molecular-based assays often demonstrate equivalent or superior sensitivity for detection of acute infection over serology as well as culture (Abele-Horn et al., 1998; Templeton et al., 2003), but this is not always the case (Michelow et al., 2004; Pitcher et al., 2006). We suggest that positive PCR assays for M. pneumoniae, especially in specimens from normally sterile sites such as spinal fluid or blood should ideally be confirmed by a second unrelated target gene, but there are no universal recommendations for this practice. The typical respiratory infection caused by M. pneumoniae is a slowly developing syndrome presenting with pharyngitis, sinus congestion, occasionally otitis media, and eventually prolonged lower respiratory involvement up to and including primary atypical pneumonia with fever and bibasilar pulmonary infiltrates. The close association betweenM. pneumoniaeand the host cells prevents the hosts mucociliary clearance mechanisms from removing the bacterium. The clinical symptoms manifested can be quite diverse with the most severe respiratory effects being CAP and occasionally abscesses (Cherry & Welliver, 1976). Atypical pneumonia is caused by atypical pathogens that are not detectable with Gram stain and cannot be cultured using standard methods. Individual spindle-shaped cells of M. pneumoniae are 12 m long and 0.10.2 m wide. Positive PCR results in serologically negative persons may be due to an inadequate immune response, early successful antibiotic treatment, or to the collection of specimens before specific antibody synthesis could occur. The observation that atypical pneumonias were often associated with cold agglutinins was made as early as 1918 (Clough & Richter, 1918), and these autoantibodies were later characterized as recognizing the I antigen of human red cells, a carbohydrate antigen of surface glycolipids and proteins (Feizi & Taylor-Robinson, 1967; Yu et al., 2001). Attachment organelles are indicated by black arrows. It also demonstrates the importance of mycoplasmal arthritis in veterinary medicine. Mycoplasma genitalium is increasingly appreciated as a common cause of sexually transmitted disease syndromes, including urethritis in men and cervicitis, endometritis, pelvic inflammatory disease, and possibly preterm birth, tubal factor infertility, and ectopic pregnancy in women. Antimicrobial management of systemic infections caused by M. pneumoniae that extend beyond the respiratory tract can be difficult, especially in persons who have antibody deficiencies or are otherwise immunocompromised. Mycoplasma pneumoniae hemadsorption and lysis of guinea pig erythrocytes that are low in endogenous catalase, are also mediated by peroxide (Tryon & Baseman, 1992). Mycoplasmas represent the smallest self-replicating organisms capable of cell-free existence, both in cellular dimensions and genome size. Nucleotide sequencing of 23S rRNA gene domains II and V and ribosomal proteins L4 and L22 showed that 10 strains had an A-to-G transition at position 2063 (M. pneumoniae numbering equivalent to 2058 in Escherichia coli numbering), one strain had A-to-C transversion at position 2063, 1 strain showed A-to-G transition at position 2064 and one a C-to-G transversion at position 2617 (M. pneumoniae numbering, or 2611 in E. coli numbering). Strong clinical data now exist linking peripheral neurologic syndromes to pathologic antibodies against carbohydrate moieties expressed on a variety of gangliosides, especially GM1 (Willison & Yuki, 2002). If CAP develops, fever in the 101103 F range is commonly seen. T.P.A. Additional reports from Japan (Suzuki et al., 2006; Morozumi et al., 2008) found macrolide resistance in 1033% of M. pneumoniae strains obtained between 2001 and 2006, all of which had mutations in domain V of 23S rRNA gene. Lower than normal body temperature (in adults older than age 65 and people with weak immune systems) Nausea . Mycoplasma genitalium is even less common in . An additional striking finding was their observation that the incidence of mycoplasmal pneumonias in hospitalized adults increased with age and it was second only to Streptococcus pneumoniae in elderly persons. It is also apparent that the impact of macrolide resistance on the outcomes of respiratory infections is not clear because the number of cases described thus far is very small and the data obtained from them are largely descriptive and difficult to quantify. In some cases, IgA is the only antibody class that is positive (Lieberman et al., 2002). Mycoplasma pneumoniae and its role as a human pathogen. It scavenges for nucleic acid precursors and apparently does not synthesize purines or pyrimidines de novo. The circular M. pneumoniae genome consists of 816 394 basepairs (bp) with 687 protein-coding genes (Himmelreich et al., 1996), about one sixth the size of Escherichia coli. Serology is a useful epidemiologic tool in circumstances where the likelihood of mycoplasmal disease is high, but it is less suited for assessment of individual patients. Search for other works by this author on: Department of Microbiology, Miami University, Oxford, OH, USA, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA, Molecular approaches to diagnosis of pulmonary diseases due to, Role of superoxide anion in host cell injury induced by, Surface localized glyceraldehyde-3-phosphate dehydrogenase of, Cross-reactive anti-galactocerebroside antibodies and, Mycoplasmas: a distinct cytoskeleton for wall-less bacteria, Evaluation of 12 commercial tests and the complement fixation test for, Antibodies to brain and other tissues in cases of, Three cases of central nervous system complications associated with. Indeed, asymptomatic pigs can become lifelong carrier. Naturally occurring resistance to tetracyclines or fluoroquinolones has never been reported in M. pneumoniae, but in vitro selection of mutants resistant to both drug classes through serial subcultures with increasing concentrations has been successful (Gruson et al., 2005; Degrange et al., 2008). 2004;17:697728. Reproduction occurs by binary fission, during which the attachment organelle migrates to the opposite pole of the cell during replication and before nucleoid separation. However, plate-type EIAs may be more efficient and cost effective in laboratories that need to measure larger numbers of specimens at the same time. This characteristic makes them naturally resistant to antibiotics that target cell wall synthesis (like the beta-lactam antibiotics ). Saving Lives, Protecting People, Incidence of community-acquired pneumonia requiring hospitalization. Hoek et al. Mutations in the quinolone resistance determining regions resulted in minimum inhibitory concentrations (MICs) for ciprofloxacin up to 32 g mL1 (Gruson et al., 2005). Electron microscopy and genome analysis confirm the absence of flagella and pili. They are most closely related to the gram-positive bacterial group that includes streptococci, bacilli, and lactobacilli. The long incubation period, relatively low transmission rate, and persistence of the organisms in the respiratory tract for variable periods following infections may explain in the prolonged duration of epidemics of M. pneumoniae infections. Mycoplasma pneumoniae has long been appreciated as a trigger for acute asthmatic attacks (Seggev et al., 1986; Leibowitz et al., 1988; Lieberman et al., 2003; Biscardi et al., 2004) and some studies have shown that the organism can be isolated in higher prevalence from asthmatics (Esposito et al., 2000; Teig et al., 2005). Subsequent to cytadherence, M. pneumoniae is believed to cause disease in part through generation of peroxide. Mast cell cytokine production is dependent upon the presence of sialic acid residues on the target cell membrane and the P1 adhesin. 1 INTRODUCTION. Importantly, oral administration with L. casei CNRZ1874 promoted M1 alveolar macrophages activation . Although recombination-mediated variation of P1 has not been demonstrated, evidence supports the occurrence of this process for a set of genes of unknown function (Dumke et al., 2004; Musatovova et al., 2008). Due to its lack of a cell wall,M. pneumoniae is extremely susceptible to desiccation. CF suffers from low sensitivity and specificity because the glycolipid antigen mixture used may be found in other microorganisms, as well as human tissues, and even plants. Clin Microbiol Rev. Since its initial description in the 1940s and eventual elucidation as a highly evolved pathogenic bacterium, Mycoplasma pneumoniae has come to be recognized as a worldwide cause of primary atypical pneumonia. The reductive evolutionary process that has led to the minimal genome of M. pneumoniae suggests that it exists as a highly specialized parasitic bacterium capable of residing in an intracellular state within the respiratory tissues, occasionally emerging to produce symptoms. Most clinical trials evaluating treatments for CAP identified small numbers of cases proven to be due to M. pneumoniae by serologic diagnosis, though some recent studies incorporated culture and/or PCR. Variation in the primary structure of the P1 adhesin is believed to play a role in the epidemiology of M. pneumoniae disease. Combined use of PCR with IgM serology may be a useful approach for diagnosis of M. pneumoniae respiratory infection in children, but potentially less useful in adults who may not mount an IgM response and would add to the expense of laboratory testing. However, others found no difference in detection of M. pneumoniae using PCR in adults (Gnarpe et al., 1997) or children (Reznikov et al., 1995) in these anatomic sites. One recent study (Ozaki et al., 2007) found that a single assay using the IgM ImmunoCard (Meridian Bioscience) had a sensitivity of only 31.8% for detection of acute M. pneumoniae infection in seropositive children with pneumonia, but this increased to 88.6% when paired sera were analyzed. These findings suggest it is risky to base diagnosis of acute mycoplasmal respiratory infection on a single assay for IgM alone. In addition to antigenic mimicry as a mechanism for autoimmunity, M. pneumoniae has been shown to directly activate cells of the immune system for cytokine production. The bacteria produce a P1 adhesin protein that allows attachment to a receptor on the respiratory tract epithelial cells. Sterols are necessary components of the triple-layered mycoplasmal cell membrane providing structural support to the osmotically fragile organisms. The varied presentation and limited diagnostic methods available present unique challenges for accurately identifyingM. pneumoniaecases and appropriately treating patients. Factors that contribute to the disease state include ciliostasis and apoptosis, resulting in localized damage to the respiratory epithelium, and an immune response which, although often robust, is poorly efficacious in terms of clearing the organism or preventing subsequent reinfections. About 515% of GuillainBarr syndrome (GBS) cases have been associated with a preceding M. pneumoniae infection (Goldschmidt et al., 1980; Hughes et al., 1999). Proteins P41 and P24, both of which are located in this region (Kenri et al., 2004), have recently been found to be required for normal relations between the attachment organelle and the cell body. Host cell lactoferrin acquisition by M. pneumoniae is yet another possible means by which local injury may occur through generation of highly reactive hydroxyl radicals resulting from the introduction of iron complexes in a microenvironment rendered locally acidic by cellular metabolism that also includes hydrogen peroxide (H2O2) and superoxide anion (Tryon & Baseman, 1987). You may develop neurological diseases if the pathogen destroys certain cells in your brain, or you may develop Crohn s colitis if thepathogen invades and destroys cells in the lower bowel. Mycoplasma pneumoniae is the most common pathogenic species infecting humans. Among 76 M. pneumoniae strains isolated between 2000 and 2003 in the northern, central, and southern regions of Japan, 13 (17%) were resistant to erythromycin, 12 of which had MICs >256 g mL1 (Matsuoka et al., 2004). This possibility is supported by recent in vitro studies suggesting that the organism can take up residence and even replicate within cultured cells for prolonged periods, but this has not been proven to occur during natural infections (Dallo & Baseman, 2000; Meseguer et al., 2003; Yavlovich et al., 2004). Immunofluorescent antibody (IFA) assays, direct and indirect hemagglutination using IgM capture, and other particle agglutination antibody assays (PAs) have been developed to detect antibody to M. pneumoniae. Positive PCR results in culture-negative persons without evidence of respiratory disease suggests inadequate assay specificity, persistence of the organism after infection, or asymptomatic carriage, perhaps in an intracellular compartment that does not yield culturable organisms. Enzyme immunoassays (EIAs) have become the most widely used commercial methods for detection of M. pneumoniae. Interestingly, Th2-dominant airway inflammation seems to potentiate the survival of the organism in lung. Histopathological examination of tissues from persons with acute mycoplasmal respiratory infection, animal models, and tracheal organ cultures demonstrate ulceration and destruction of ciliated epithelium of bronchi and bronchioles, edema, bronchiolar and alveolar infiltrates of macrophages, lymphocytes, neutrophils, plasma cells, and fibrin. It is among the. Reference laboratories may also offer assays they have validated themselves using various gene targets. Mycoplasma genitalium is described as a "stealth" pathogen, so most people don't show any visible symptoms.In fact, a recent study in Britain showed that 94.4% of men and 56.2% of women with . The CARDS toxin most likely aids in the colonization and pathogenic pathways ofM. pneumoniae, leading to inflammation and airway dysfunction. Disease severity may not justify invasive procedures to obtain lower respiratory tract specimens. Of particular interest was the behaviour of Mycoplasma mycoides ssp. Evidence linking these cases with autoantibodies is weaker than the association with GBS but some data exist (Nishimura et al., 1996; Komatsu et al., 1998). They found that 22.8% blood donors and 53.8% of patients with various non-Mycoplasma infections were positive for IgA, raising doubts about its value to support serodiagnosis of a current M. pneumoniae infection. Prior allergic sensitization of mice to hen egg ovalbumin is associated with downregulation of TLR2 expression and decreased clearance of M. pneumoniae in mouse lung (Chaplin et al., 2007; Wu et al., 2008). Recent studies (Henderson & Jensen, 2006; Seybert et al., 2006) reveal this core to consist of a pair of nonequivalent parallel rods with numerous cross-striations, connected to the tip of the attachment organelle through a terminal button. 1 Mycoplasma pneumoniae (M. p), Chlamydiae psittaci pneumoniae (C. p) and Legionella spp pneumoniae (L. p) are common causes in atypical pneumonia among immune-competent hosts. The two subtypes of M. pneumoniae most frequently isolated from clinical specimens differ to some extent in the amino acid and nucleotide sequences of P1 and its coding gene (Su et al., 1990), though numerous further variants have been identified in recent years (Kenri et al., 1999; Dorigo-Zetsma et al., 2000, 2001; Dumke et al., 2004; Pereyre et al., 2007). 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