Rising Rates of Macrolide-Resistant Mycoplasma pneumoniae in the Central United States

Yamada, Masaki; Buller, Richard S.; Bledsoe, Stephanie; Storch, Gregory A.

doi:10.1097/inf.0b013e318247f3e0

Cited by 76 publications

(53 citation statements)

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“…We identified an overall rate of macrolide resistance of 10% among specimens collected be- (10). This is similar to the prevalence of resistance observed in the current study.…”

Section: Discussionsupporting

confidence: 78%

“…In M. pneumoniae infections, macrolide resistance is an emerging threat worldwide, and in some parts of the world, Ͼ90% of M. pneumoniae infections are caused by resistant strains (6,7). In the United States, the incidence of infection with macrolide-resistant M. pneumoniae strains is not well defined, although the trait has been consistently reported over the past decade (8)(9)(10). Macrolide-resistant M. pneumoniae infection has been associated with increased febrile period, increased duration of persistent cough, and extended antibiotic therapy compared to macrolide-sensitive strains (11)(12)(13)(14)(15)(16).…”

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confidence: 99%

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Investigations of Mycoplasma pneumoniae Infections in the United States: Trends in Molecular Typing and Macrolide Resistance from 2006 to 2013

2015

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Mycoplasma pneumoniae is a leading cause of respiratory infections, including community-acquired pneumonia (CAP). Currently, pathogen-specific testing is not routinely performed in the primary care setting, and the United States lacks a systematic surveillance program for M. pneumoniae. Documentation of individual cases and clusters typically occurs only when severe illness and/or failure to improve with empirical antibiotic therapy is observed. Outbreaks, some lasting for extended periods and involving a large number of cases, occur regularly. However, many more likely go unrecognized due to the lack of diagnostic testing and structured reporting. We reviewed data from 17 investigations of cases, small clusters, and outbreaks of M. pneumoniae M ycoplasma pneumoniae is a common respiratory pathogen in adults and children worldwide and is a leading cause of community-acquired pneumonia (CAP). The majority of infections are self-limiting, and empirical treatment without pathogen-specific diagnostic testing is common in the primary care setting. In fact, the current treatment guidelines do not recommend diagnostic testing for suspected CAP of atypical bacterial etiology in adults in the outpatient setting unless a change in the patient treatment regimen is anticipated (1). The recommendation to perform diagnostic testing for M. pneumoniae infection in children is classified as a weak recommendation and likely not routinely performed, in part due to a lack of available diagnostic tests in the primary care setting and at state and local public health laboratories (2). The estimates of the actual number of cases occurring annually are inexact due to the lack of systematic surveillance and reporting. Although historically noted to occur in 3-to 7-year cycles, outbreaks of M. pneumoniae are common and may last for several months as a result of the long incubation period and prolonged carriage after resolution of symptoms (3-5).Excessive or inappropriate antibiotic use provides selective pressure for the development of antimicrobial resistance. In M. pneumoniae infections, macrolide resistance is an emerging threat worldwide, and in some parts of the world, Ͼ90% of M. pneumoniae infections are caused by resistant strains (6, 7). In the United States, the incidence of infection with macrolide-resistant M. pneumoniae strains is not well defined, although the trait has been consistently reported over the past decade (8-10). Macrolide-resistant M. pneumoniae infection has been associated with increased febrile period, increased duration of persistent cough, and extended antibiotic therapy compared to macrolide-sensitive strains (11-16).Methods for molecular typing of M. pneumoniae strains have been developed, including discrimination of two major types and variants based on the sequence of the P1 adhesion molecule gene and identification of multiple types using multilocus variablenumber tandem-repeat analysis (MLVA) to examine four or five polymorphic loci. Despite development of these sophisticated typing methods, character...

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“…We identified an overall rate of macrolide resistance of 10% among specimens collected be- (10). This is similar to the prevalence of resistance observed in the current study.…”

Section: Discussionsupporting

confidence: 78%

mentioning

confidence: 99%

Investigations of Mycoplasma pneumoniae Infections in the United States: Trends in Molecular Typing and Macrolide Resistance from 2006 to 2013

2015

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“…However, macrolide-resistant (MR) M. pneumoniae has been reported in Japan since 2000 and has become widespread in Japan and China (1)(2)(3)(4)(5)(6)(7). MR M. pneumoniae is now spreading throughout Europe and North America, especially in children (8)(9)(10)(11)(12)(13). The most frequent mechanism of resistance is an A-to-G mutation at position 2063 of M. pneumoniae 23S rRNA domain V (A2063G) (5).…”

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confidence: 99%

Therapeutic Efficacy of Macrolides, Minocycline, and Tosufloxacin against Macrolide-Resistant Mycoplasma pneumoniae Pneumonia in Pediatric Patients

Kawai

Miyashita

Kubo

et al. 2013

Antimicrob Agents Chemother

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The importance of macrolide-resistant (MR) Mycoplasma pneumoniae has become much more apparent in the past decade. We investigated differences in the therapeutic efficacies of macrolides, minocycline, and tosufloxacin against MR M. pneumoniae. A total of 188 children with M. pneumoniae pneumonia confirmed by culture and PCR were analyzed. Of these, 150 patients had a strain with an MR gene and 134 had one with an A-to-G mutation at position 2063 of M. pneumoniae 23S rRNA domain V. Azithromycin (n ‫؍‬ 27), clarithromycin (n ‫؍‬ 23), tosufloxacin (n ‫؍‬ 62), or minocycline (n ‫؍‬ 38) was used for definitive treatment of patients with MR M. pneumoniae. Defervescence within 48 h after the initiation of antibiotic therapy was observed in 41% of the patients in the azithromycin group, 48% of those in the clarithromycin group, 69% of those in the tosufloxacin group, and 87% of those in the minocycline group. The average number of days of fever after the administration of antibiotic treatment was lower in the minocycline and tosufloxacin groups than in the macrolide groups. The decrease in the M. pneumoniae burden, as estimated by the number of DNA copies, after 48 to 96 h of treatment was more rapid in patients receiving minocycline (P ‫؍‬ 0.016) than in those receiving tosufloxacin (P ‫؍‬ 0.049), azithromycin (P ‫؍‬ 0.273), or clarithromycin (P ‫؍‬ 0.107). We found that the clinical and bacteriological efficacies of macrolides against MR M. pneumoniae pneumonia was low. Our results indicated that minocycline rather than tosufloxacin can be considered the first-choice drug for the treatment of M. pneumoniae pneumonia in children aged >8 years.

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“…Mycoplasma pneumoniae is a causative pathogen of human bronchitis and walking pneumonia. Outbreaks of M. pneumoniae infections occur frequently in many parts of the world, and the increase in the incidence of macrolideresistant M. pneumoniae infections is a growing problem (3)(4)(5). M. pneumoniae exhibits "gliding motility" in the direction of the leading-edge cell protrusion at a maximum speed of 1 m (onehalf of its cell length) per second (6)(7)(8)(9).…”

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confidence: 99%

Structural Study of MPN387, an Essential Protein for Gliding Motility of a Human-Pathogenic Bacterium, Mycoplasma pneumoniae

et al. 2016

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Mycoplasma pneumoniae is a human pathogen that glides on host cell surfaces with repeated catch and release of sialylated oligosaccharides. At a pole, this organism forms a protrusion called the attachment organelle, which is composed of surface structures, including P1 adhesin and the internal core structure. The core structure can be divided into three parts, the terminal button, paired plates, and bowl complex, aligned in that order from the front end of the protrusion. To elucidate the gliding mechanism, we focused on MPN387, a component protein of the bowl complex which is essential for gliding but dispensable for cytadherence. The predicted amino acid sequence showed that the protein features a coiled-coil region spanning residue 72 to residue 290 of the total of 358 amino acids in the protein. Recombinant MPN387 proteins were isolated with and without an enhanced yellow fluorescent protein (EYFP) fusion tag and analyzed by gel filtration chromatography, circular dichroism spectroscopy, analytical ultracentrifugation, partial proteolysis, and rotary-shadowing electron microscopy. The results showed that MPN387 is a dumbbell-shaped homodimer that is about 42.7 nm in length and 9.1 nm in diameter and includes a 24.5-nm-long central parallel coiled-coil part. The molecular image was superimposed onto the electron micrograph based on the localizing position mapped by fluorescent protein tagging. A proposed role of this protein in the gliding mechanism is discussed. IMPORTANCEHuman mycoplasma pneumonia is caused by a pathogenic bacterium, Mycoplasma pneumoniae. This tiny, 2-m-long bacterium is suggested to infect humans by gliding on the surface of the trachea through binding to sialylated oligosaccharides. The mechanism underlying mycoplasma "gliding motility" is not related to any other well-studied motility systems, such as bacterial flagella and eukaryotic motor proteins. Here, we isolated and analyzed the structure of a key protein which is directly involved in the gliding mechanism.M ycoplasma members represent a group of parasitic and, occasionally, commensal bacteria that lack a peptidoglycan layer and have small genomes (1, 2). Mycoplasma pneumoniae is a causative pathogen of human bronchitis and walking pneumonia. Outbreaks of M. pneumoniae infections occur frequently in many parts of the world, and the increase in the incidence of macrolideresistant M. pneumoniae infections is a growing problem (3-5). M. pneumoniae exhibits "gliding motility" in the direction of the leading-edge cell protrusion at a maximum speed of 1 m (onehalf of its cell length) per second (6-9). Detailed analyses of gliding in M. pneumoniae have shown that the gliding cells move continuously and pivot around the protrusion (7). This motility, combined with the ability to adhere to epithelial cells, is involved in the infection process, enabling the bacteria to translocate from the tip of bronchial cilia to the host cell surface (10). Previous studies, including genome analyses, have shown that this motility is not related...

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Rising Rates of Macrolide-Resistant Mycoplasma pneumoniae in the Central United States

Cited by 76 publications

References 12 publications

Investigations of Mycoplasma pneumoniae Infections in the United States: Trends in Molecular Typing and Macrolide Resistance from 2006 to 2013

Investigations of Mycoplasma pneumoniae Infections in the United States: Trends in Molecular Typing and Macrolide Resistance from 2006 to 2013

Therapeutic Efficacy of Macrolides, Minocycline, and Tosufloxacin against Macrolide-Resistant Mycoplasma pneumoniae Pneumonia in Pediatric Patients

Structural Study of MPN387, an Essential Protein for Gliding Motility of a Human-Pathogenic Bacterium, Mycoplasma pneumoniae

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