Emerging Pathogenic Respiratory Mycoplasma hominis Infections in Lung Transplant Patients: Time to Reassesses it's Role as a Pathogen?

Identification of sacrococcygeal and pelvic abscesses infected with invasive Mycoplasma hominis by MALDI‐TOF MS

“…This special biological characteristic makes it can not only escape the routine etiological examination such as Gram staining, but also escape the clinician's empirical anti‐infection treatment. The growth rate of Mycoplasma on the blood agar medium routinely used for pathogen proliferation is slower than that of common bacteria, it usually takes 48 h or even longer, and the colony morphology is not typical 13,14 . Undetected report or untimely pathogen identification may cause an aggravation of the inflammation and lead to poor outcomes of complications and prolonged hospital stays.…”

Lung Abscess and Recurrent Empyema After Infection With Mycoplasma hominis: A Case Report and Review of the Literature

“…Mycoplasma hominis is sporadically associated with a broad range of extragenital infections, eg, mediastinitis or endocarditis, bone/joint infections, intrauterine infections, or other abscesses [ 18 , 21 , 22 ]. This may suggest that significant respiratory pathology by “urogenital” mycoplasmas may be more common than generally believed, but it is often simply missed by routine microbiological work-up [ 18 ].…”

“…Because thoracic surgery patients in general often suffer from underlying chronic respiratory disease, for example, COPD, an increased vulnerability of these patients and especially lung transplant patients can be assumed. The routinely used perioperative bacterial prophylaxis antibiotics, for example, cefepime, are ineffective against M hominis [ 18 ]. Moreover, most of the current regimens for empirical therapy of posttransplant infectious complications do not cover M hominis .…”

“…Most of the typical broad-spectrum antimicrobial agents are ineffective against M hominis [ 18 ]. Mycoplasmas are inherently resistant to beta-lactam-based (eg, penicillins, cephalosporins and carbapenems) or glycopeptide antibiotics (eg, vancomycin) as well as antimetabolites (eg, trimethoprim/sulfamethoxazole) or lipopolysaccharide-targeting antibiotics (eg, polymyxin) [ 18 , 19 ] because they lack a cell wall.…”

“…Most of the typical broad-spectrum antimicrobial agents are ineffective against M hominis [ 18 ]. Mycoplasmas are inherently resistant to beta-lactam-based (eg, penicillins, cephalosporins and carbapenems) or glycopeptide antibiotics (eg, vancomycin) as well as antimetabolites (eg, trimethoprim/sulfamethoxazole) or lipopolysaccharide-targeting antibiotics (eg, polymyxin) [ 18 , 19 ] because they lack a cell wall. Moreover, M hominis is unique in its resistance to macrolides (eg, azithromycin), because the sequence of the M hominis single copy of 23S ribosomal ribonucleic acid has a G2057A transition, leading to a replacement of a guanidine with an adenine at a position known to abrogate macrolide binding to the ribosome [ 20 ].…”