Mycoplasma genitalium

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Mycoplasma genitalium
3D Whole Cell (3D-WC) model of a Mycoplasma genitalium cell
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Mycoplasmatota
Class: Mollicutes
Order: Mycoplasmoidales
Family: Mycoplasmoidaceae
Genus: Mycoplasmoides
Species:
M. genitalium
Binomial name
Mycoplasmoides genitalium
(Tully et al. 1983) Gupta et al. 2018[1]
Synonyms

Mycoplasma genitalium Tully et al. 1983[2]

Mycoplasma genitalium (also known as MG

antibiotics.[6][11]

Symptoms of infection

Mgen is a bacterium recognized for causing urethritis in both men and women along with cervicitis and pelvic inflammation in women.[12] It presents clinically similar symptoms to that of Chlamydia trachomatis infection and has shown higher incidence rates, compared to both Chlamydia trachomatis and Neisseria gonorrhoeae infections in some populations.[13]

Infection with Mgen can be symptomatic or asymptomatic. Both men and women may experience inflammation in the urethra (urethritis), characterized by mucopurulent discharge in the urinary tract, and burning while urinating. In women, it causes cervicitis and pelvic inflammatory diseases (PID), including endometritis and salpingitis.[12] Women may also experience bleeding after sex and it is also linked with tubal factor infertility.[5][14][15] For men, the most common signs are painful urination or a watery discharge from the penis.[16]

There is a consistent association of M. genitalium infection and female reproductive tract syndromes. M. genitalium infection was significantly associated with increased risk of preterm birth, spontaneous abortion, cervicitis, and pelvic inflammatory disease. In addition, this pathogen may latently infect the chorionic villi tissues of pregnant women, thereby impacting pregnancy outcome.[17] Infertility risk is also strongly associated with infection with M. genitalium, although evidence suggests it is not associated with male infertility.[18] When M. genitalium is a co-infectious agent risk associations are stronger and statistically significant.[19]

lymphomas in some individuals. These studies have yet to find conclusive evidence to suggest a link.[23]

Genome

Gene map of Mycoplasma genitalium. Circularly arranged coloured bands are the protein-coding genes and other loci in their position in the DNA. The genome has 580,070 base pairs
(580 kb).
3D model of the Mycoplasma genitalium cell obtained with CellPACKgpu. The horizontal clipping plane shows the cytoplasmic environment on top and the membrane with associated proteins in the bottom. An additional clipping plane carves out a cubic section of the model, magnified on the right. Proteins colored by biological function.

The genome of M. genitalium strain G37T consists in one circular DNA of 580,070

energy metabolism. It was the second complete bacterial genome ever sequenced, after Haemophilus influenzae.[24] Later data from KEGG reports 476 protein-coding genes and 43 RNA genes, totaling 519.[27] It is unclear where the "525" gene count for the G37T stems from and what gene calling procedure was used.[28]

In 2006, the team at the J. Craig Venter Institute reported that only 382 genes are essential for biological functions.

The Minimal Genome Project, a study to find the smallest set of genetic material necessary to sustain life.[30]

There is limited divergence among clinical strains of M. genitalium. All strains retain the small genome size.[31]

Diagnosis

Recent research shows that prevalence of Mgen is currently higher than other commonly occurring

fluoroquinolone.[37]

According to the European guidelines, the indication for commencement of diagnosis for Mgen infection are:[35]

  1. Detection of nucleic acid (DNA and/or RNA) specific for Mgen in a clinical specimen
  2. Current partners of individuals who tested positive for Mgen should be treated with the same antimicrobial as the
    index patient
  3. If current partner does not attend for evaluation and testing, treatment with the same regimen as given to the index patient should be offered on epidemiological grounds
  4. On epidemiological grounds for sexual contacts in the previous 3 months; ideally, specimens for a Mgen NAAT should be collected before treatment and treatment should not be given before the result are available

Screening for Mgen with a combination of detection and macrolide resistance mutations will provide the adequate information required to develop personalised antimicrobial treatments, in order to optimise patient management and control the spread of antimicrobial resistance (AMR).[35][38]

Detection of resistance

Owing to the widespread macrolide resistance, samples that are positive for Mgen should ideally be followed up with an assay capable of detecting mutations that mediate antimicrobial resistance. The European Guideline on Mgen infections, in 2016,[39] recommended complementing the molecular detection of Mgen with an assay capable of detecting macrolide resistance-associated mutations.[citation needed]

Treatment

The U.S. Centers for Disease Control and Prevention recommends a step-wise treatment approach for Mycoplasma genitalium with doxycycline for 7 days followed immediately by a 7-day course of moxifloxacin as the preferred therapy due to high rates of macrolide resistance.[40][41][42] If resistance assay testing is available, and the Mgen is sensitive to macrolides, the CDC recommends a 7-day course of doxycycline followed by a 4-day course of azithromycin.[40] Although the majority of M. genitalium strains are sensitive to moxifloxacin, resistance has been reported, and potential for serious, adverse side effects should be considered with this regimen. [43] Floroquinolones, including Moxifloxacin, have been associated with disabling and potentially irreversible serious adverse reactions that have occurred together including:[citation needed]

  • Tendinitis and tendon rupture
  • Peripheral Neuropathy
  • Central nervous system effects

and other serious side effects detailed in the FDA black box warning. Moxifloxacin/Avelox should be reserved for use when patients have no other treatment options. [44]

In settings without access to resistance testing, or if Moxifloxacin cannot be used, the CDC recommends as an alternative regimen: 7 days of doxycycline followed by the 4-day course of azithromycin, with a test of cure 21 days after treatment being required due to the high rate of macrolide resistance.

Beta lactam antibiotics are not effective against Mgen as the organism lacks a cell wall.[42]

In the UK the British Association for Sexual Health and HIV (BASHH) guidelines for treatment are:[45]

  • Doxycycline 100mg twice a day for seven days followed by azithromycin 1 gram orally as a single dose then 500mg orally once daily for 2 days where organism is known to be macrolide-sensitive or where resistance status is unknown.
  • Moxifloxacin 400mg orally once daily for 10 days if organism known to be macrolide-resistant or where treatment with azithromycin has failed.

Treatment of Mycoplasma genitalium infections is becoming increasingly difficult due to rapidly growing antimicrobial resistance.[46] Diagnosis and treatment is further hampered by the fact that Mycoplasma genitalium infections are not routinely tested.[47] Studies have demonstrated that a 5-day course of azithromycin has a superior cure rate compared to a single, larger dose. Further, a single dose of azithromycin can lead to the bacteria becoming resistant to azithromycin.[48] Among Swedish patients, doxycycline was shown to be relatively ineffective (with a cure rate of 48% for women and 38% for men); and treatment with a single dose of azithromycin is not prescribed due to it inducing antimicrobial resistance. The five-day treatment with azithromycin showed no development of antimicrobial resistance.[49] Based on these findings, UK doctors are moving to the 5-day azithromycin regimen. Doxycycline is also still used, and moxifloxacin is used as a second-line treatment in case doxycyline and azithromycin are not able to eradicate the infection.[50][51] In patients where doxycycline, azithromycin and moxifloxacin all failed, pristinamycin has been shown to still be able to eradicate the infection.[50]

History

Mycoplasma genitalium was originally isolated in 1980 from

energy-generating pathways, although it shared a core genome of ~250 protein-encoding genes.[55]

In 2018, Gupta et al. proposed to change the name of Mycoplasma genitalium to Mycoplasmoides genitalium on phylogenetic grounds, reflecting the existing knowledge that M. genitalium is not very related to other Mycoplasma.[1] The change became correct name under the International Code of Nomenclature of Prokaryotes (ICNP, "Code") with Validation List 184, published by the ICSP ("Committee").[56] Mycoplasmaologists working in the field generally oppose this renaming. In 2019, they published an opinion paper arguing that even though the phylogenetic methods are valid, Gupta's renaming scheme causes too many changes, which is impractical and confusing.[57] They cite some essential principles of the Code, such as "no unnecessary new names", "aim at stability of names", and "avoid or reject the use of names which may cause error or confusion".[57] However, the 2019 argument for preserving old names was rejected by the Committee in Opinion 122 of 2022,[58] where it was ruled that the argument incorrectly cited the Code.[56] The Opinion emphasizes that use of an older validly published name remains acceptable under the Code.[58]

Synthetic genome

On 6 October 2007,

kilodaltons (kDa). Printed in 10-point font, the letters of the genome cover 147 pages.[63]

On 20 July 2012, Stanford University and the J. Craig Venter Institute announced successful simulation of the complete life cycle of a Mycoplasma genitalium cell, in the journal Cell.[64] The entire organism is modeled in terms of its molecular components, integrating all cellular processes into a single model. Using object oriented programming to model the interactions of 28 categories of molecules, including DNA, RNA, proteins, and metabolites, and running on a 128 computer Linux cluster, the simulation takes 10 hours for a single M. genitalium cell to divide once—about the same time the actual cell takes—and generates half a gigabyte of data.[65]

Research

The discovery of

antibodies from multiple myeloma patients' blood were recognised by M. genitalium. The antibody reactivity was due to a protein never known before, and is chemically responsive to all types of human and nonhuman antibodies available. The protein is about 50 kDa in size, and composed of 556 amino acids.[67] Mgen evolved from a gram-positive ancestor that was clostridium-like but has lost the genes to code for the enzymes involved in de novo nucleic acid synthesis, amino acid synthesis, and synthesis of fatty acids.[68] This means that Mgen needs the host's growth factors to keep reproducing. Although Mgen has abilities that help it adhere to cells, it is still unknown how the bacteria can maintain an infection inside the epithelial cells of the ectocervix and vagina when shedding of the apical layer of cells occur. The organism's ability to have adhesion to host cells relies of two proteins, P110 and P140. Adhesion is an important step in beginning an infection in a cell and Mgen can adhere to spermatozoa, erythrocytes, and epithelial cells. The terminal organelle relies on these proteins as well because without them the organelle was not present. The segmented pair plates of Mgen [vague] is a core of dense electrons which is anchored to the cell membrane. The end of this core is in contact with the wheel complex and the wheel complex contains the proteins MG219, MG200, MG386, and MG491 which aid in the gliding motility of the bacteria. Although Mgen lacks secreted virulence factors, the protein MG186 degrades host nucleic acids due to it being a calcium-dependent membrane-associated nuclease.[citation needed
]

See also

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External links

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