Current understanding and treatment of intra‐amniotic infection with Ureaplasma spp.

Abstract

Considerable evidence has shown that intra-amniotic infection with Ureaplasma spp. increases the risk of chorioamnionitis and preterm labor. Ureaplasma spp. are among the smallest organisms, and their isolation is uncommon in routine clinical practice because of their size and high auxotrophy. Although Ureaplasma spp. have been reported as causative agents of preterm birth, they also have a high incidence in vaginal swabs collected from healthy reproductive-age women; this has led to questions on the virulence of Ureaplasma spp. and to them being considered as harmless commensal bacteria. Therefore, many efforts have been made to clarify the pathogenicity of Ureaplasma spp. at the molecular level. Ureaplasma spp. are surrounded by lipoproteins, including multiple-banded antigen. Both multiple-banded antigen and its derivative, that is, the synthetic lipopeptide, UPM-1, induce an inflammatory response in a preterm mice model, which was adequate to cause preterm birth or stillbirth. In this review, we present an overview of the virulence mechanisms of Ureaplasma spp. and treatment of ureaplasma infection during pregnancy to prevent possible serious sequelae in infants. In addition, relevant mechanisms underlying antibiotic resistance in Ureaplasma spp. are discussed. Ureaplasma spp. are naturally resistant against β-lactam antibiotics because of the lack of a cell wall. Azithromycin is one of the effective agents that can control intrauterine ureaplasma infection. In fact, macrolide-and fluoroquinolone-resistant isolates of Ureaplasma spp. have already been observed in perinatal practice in Japan.

Infection strategies of mycoplasmas: Unraveling the panoply of virulence factors

“…Based on the available data, mycoplasmas utilize three mechanisms for degrading Ig. The first mechanism is the secretion of IgA protease, as reported in U. urealyticum and U. parvum, which participates in facilitating microorganism colonization and host immune system evasion on the mucosal surface by proteolytic activity against IgA 1 [15,[138][139][140]. The second mechanism is retaining the Ig binding protein and Ig protease (MIB-MIP) system to degrade IgG.…”

“…Other potential pathogenic effects of NH 3 production including fatal hyperammonemia syndrome and the formation and precipitation of struvite in the urinary tract [200,201]. A study also showed that the urease activity of U. urealyticum was higher than that of U. parvum [15], suggesting that U. urealyticum may trigger more severe localized pathological damage.…”

“…Mycoplasmas can also express various pathogenic enzymes such as lipolytic enzymes, peptidases, phosphatases, ecto-ATPases, cytotoxic nucleases and nucleotidases, that are considered important mycoplasma pathogenic factors [12,13]. Furthermore, some inherent components located at the mycoplasma cell membrane, such as lipids, membrane lipoproteins, and even superantigens produced by Mycoplasma arthritidis, could trigger an inflammatory response through various strategies (Figure 1) [14][15][16]. Although several questions remain unanswered, significant progress has been made in identifying the virulence factors by which mycoplasmas interact with and subsequently damage the host cells.…”

Validation of the loop-mediated isothermal amplification method for rapid and sensitive detection of Ureaplasma species in respiratory tracts of preterm infants

“…Ureaplasma spp. are frequently isolated from the amniotic fluid and placentas of preterm infants [1,2] and have been associated with adverse prenatal outcomes such as miscarriages, preterm labor, preterm premature rupture of membranes, and chorioamnionitis [3].…”

In-vitro activity of lipoic acid against Ureaplasma urealyticum and Ureaplasma parvum isolated from women with infections of the urogenital tract. A pilot study

“…The lack of a cell wall confers resistance to all β-lactam and glycopeptide antibiotics. On the other hand, the lack of de novo synthesis of folic acid makes the cells resistant to diaminopyrimidines and sulfonamides (Beeton & Spiller, 2016;Tantengco & Yanagihara, 2019). Many authors emphasize that the development of resistance of Ureaplasma spp.…”