Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety

Baseman, Joel B.; Tully, Joseph G.

doi:10.3201/eid0301.970103

Cited by 293 publications

(263 citation statements)

References 65 publications

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“…Mycoplasmas have been held responsible for human diseases, such as pneumonia, arthritis, and urethritis 38 . More recently, they have also been implicated in the progression of AIDS, chronic fatigue syndrome, acute respiratory distress syndrome, and others 39 .…”

Section: Discussionmentioning

confidence: 99%

“…More recently, they have also been implicated in the progression of AIDS, chronic fatigue syndrome, acute respiratory distress syndrome, and others 39 . However, these arguments have not succeeded in sensitizing scientists in regard to a pathogenetic relation, because most of these arguments are based on case reports whose positivity for mycoplasmas results from serological data, culture, or PCR 40,41 . Few studies sought M. pneumoniae in atherosclerotic plaques, and the results were negative 42 or slightly positive 43 .…”

Section: Discussionmentioning

confidence: 99%

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Coinfection with Mycoplasma Pneumoniae and Chlamydia Pneumoniae in ruptured plaques associated with acute myocardial infarction

Higuchi¹,

Reis²,

Sambiase³

et al. 2003

Arq. Bras. Cardiol.

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OBJECTIVE: To study atheromas, Mycoplasma pneumoniae (M. pneumoniae), and Chlamydia pneumoniae (C. pneumoniae). METHODS: C. pneumoniae was studied with immunohistochemistry and M. pneumoniae with in situ hybridization (ISH), in segments of coronary arteries (SCA) as follows: group A - thrombosed ruptured plaques (TRP) of 23 patients who died due to acute myocardial infarction (AMI); group B - 23 nonruptured plaques (NRP) of group A patients; group C - NRP of 11 coronary patients who did not die due to AMI; and group D - 11 SCA from patients with dilated cardiomyopathy or Chagas' disease without atherosclerosis. RESULTS: The mean number of C. pneumoniae+ cells/400x in groups A, B, C, and D was, respectively, 3.3±3.6; 1.0±1.3; 1.2±2.4; and 0.4±0.3; and the percentage of M. pneumoniae area was, respectively, 3.9±3.5; 1.5± 1.6; 0.9±0.9; and 0.4±0.2. More M. pneumoniae and C. pneumoniae were found in of group A than in group B (P<0.01). Good correlation was seen between the area of the vessel and the M. pneumoniae area in the plaque (r = 0.46; P=0.001) and between C. pneumoniae+ cells and CD4+ T lymphocytes (r = 0.42; P<0.01). The number of C. pneumoniae+ cells correlated with CD20+ B cells (r=0.48; P<0.01). CONCLUSION: M. pneumoniae and C. pneumoniae are more frequently found in TRP correlate with the intensity of the inflammation and diameter of the vessel (positive remodeling)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Coinfection with Mycoplasma Pneumoniae and Chlamydia Pneumoniae in ruptured plaques associated with acute myocardial infarction

Higuchi¹,

Reis²,

Sambiase³

et al. 2003

Arq. Bras. Cardiol.

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“…These parasitic micro-organisms have been continuously reemerging as important human and animal pathogens (Baseman & Tully, 1997). In particular, Mycoplasma genitalium has been linked to numerous genitourinary as well as extragenitourinary human pathologies (Baseman et al, 1988) and it is a leading cause of Chlamydia -negative, non-gonococcal urethritis (Taylor-Robinson & Horner, 2001;Tully et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Role of Mycoplasma genitalium MG218 and MG317 cytoskeletal proteins in terminal organelle organization, gliding motility and cytadherence

et al. 2008

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The terminal organelle is a differentiated structure that plays a key role in mycoplasma cytadherence and locomotion. For this reason, the analysis of Mycoplasma genitalium mutants displaying anomalous terminal organelles could improve our knowledge regarding the structural elements required for proper locomotion. In this study, we isolated several M. genitalium mutants having transposon insertions within the mg218 or mg317 genes, which encode the orthologues of Mycoplasma pneumoniae HMW2 and HMW3 cytoskeletal proteins, respectively. As expected, mg218 " and mg317 " mutants exhibit a reduced gliding motility, although their ability to attach to solid surfaces was not completely abolished. Interestingly, most of the mg218 " mutants expressed N-terminal MG218 derivatives and showed the presence of short terminal organelles retaining many of the functions displayed by this structure in the wild-type strain, suggesting that the N-terminal region of this protein is an essential element in the architecture of the terminal organelle. Separately, the analysis of mg317 " mutants indicates that MG317 protein is involved in the formation of the terminal button and contributes to anchoring the electron-dense core to the cell membrane. The results presented here clearly show that MG218 and MG317 proteins are implicated in the maintenance of gliding motility and cytadherence in M. genitalium.

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“…The best-studied mycoplasmas of vertebrate hosts are pathogens of humans and domesticated animals. These pathogens are usually associated with subclinical or subtle, slowly progressive or chronic diseases (3). Pathogenicity in all hosts is poorly understood beyond the generalization that host responses to mycoplasmal cytadherence exacerbate disease, and variation in cell surface antigens can occur with high frequency in some mycoplasmas (34).…”

Section: Discussionmentioning

confidence: 99%

Spreading Factors of Mycoplasma alligatoris , a Flesh-Eating Mycoplasma

Brown¹,

Zacher²,

Farmerie

2004

J Bacteriol

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Mycoplasma alligatoris causes lethal invasive disease of alligators and caimans. A homolog of the nagH gene, encoding a hyaluronidase secreted by Clostridium perfringens, and a C. perfringens hyaluronidase nagI or nagK pseudogene were discovered in the M. alligatoris genome. The nagH gene was detected by PCR in the closest relative of M. alligatoris, Mycoplasma crocodyli, but not in 40 other species representing the Mycoplasma hominis, Mycoplasma pneumoniae, and Spiroplasma phylogenetic clusters. The hyaluronidase activity in the cellular fraction of M. alligatoris and M. crocodyli SP4 broth cultures was equivalent to 10 ؊16 U of Streptomyces hyalurolyticus hyaluronidase CFU ؊1 . Negligible activity was present in the cell-free supernatant fraction. No chondroitinase activity was detected. There is also a novel homolog of the nanI gene, which encodes a sialidase secreted by C. perfringens, in the M. alligatoris genome. The signature YRIP and SXDXGXTW motifs and catalytic residues of the clostridial sialidase are conserved in the mycoplasmal gene, but the leader sequence necessary for its secretion by C. perfringens is absent. The gene was not detected by PCR in any other mycoplasma. Potent cell-associated sialidase activity was present in M. alligatoris colonies on agar but not in the cell-free supernatants of broth cultures or in M. crocodyli. The presence of hyaluronidase and sialidase in M. alligatoris is consistent with the rapid invasiveness and necrotizing effects of this organism, and the lack of sialidase in M. crocodyli is consistent with its comparatively attenuated virulence. This genetic and biochemical evidence suggests that the spreading factors hyaluronidase and sialidase, a combination unprecedented in mycoplasmas, are the basis of the virulence of M. alligatoris.Mycoplasma alligatoris causes a lethal invasive disease in adult alligators (Alligator mississippiensis) and closely related caimans (Caiman latirostris). The pathology observed as early as 1 week after infection by instillation via the glottis includes necrotizing pneumonia, severe pericarditis, necrotizing myocarditis, lymphocytic interstitial nephritis, lymphocytic periportal hepatitis, splenic hyperplasia, pyogranulomatous meningitis, and necrotizing synovitis (9,10,11,13,18,33). Hatchling alligators also rapidly developed disseminated M. alligatoris mycoplasmosis after intratracheal instillation, and the lesions are similar to those of adults and include acute multifocal brainstem hemorrhage (35). Mycoplasma crocodyli (23), the closest known relative of M. alligatoris (98% 16S rRNA gene similarity [9]), causes a similar necrotizing synovitis and occasionally subacute pneumonia in Nile crocodiles (Crocodylus niloticus) (27,28). The severity of the lesions correlates with the numbers of M. alligatoris cells in affected tissues, suggesting that a spreading factor(s) contributes to the virulence. The extracellular matrix (ECM)-degrading enzymes that act as bacterial spreading factors include hyaluronidases, sialidases, and mucinases (26...

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Mycoplasmas: Sophisticated, Reemerging, and Burdened by Their Notoriety

Cited by 293 publications

References 65 publications

Coinfection with Mycoplasma Pneumoniae and Chlamydia Pneumoniae in ruptured plaques associated with acute myocardial infarction

Coinfection with Mycoplasma Pneumoniae and Chlamydia Pneumoniae in ruptured plaques associated with acute myocardial infarction

Role of Mycoplasma genitalium MG218 and MG317 cytoskeletal proteins in terminal organelle organization, gliding motility and cytadherence

Spreading Factors of Mycoplasma alligatoris , a Flesh-Eating Mycoplasma

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