Mycoplasma hominis is a facultative urogenital commensal organism reported to be present in 75% of women and 29% of men causing pelvic inflammatory disease, urinary tract infection (UTI), urethritis, and cervicitis [1], in addition to extragenital infection such as pneumonia and septic arthritis and other immunocompromised patients [2, 3]. Also, M. hominis has been reported in 8% of patients with chronic respiratory disease. Recently, several cases reported the presence of M. hominis in transplant recipients, which can be donor-driven as the organism is present in the respiratory secretion in 1–3% of individuals [4]. In the two cases presented, the source of infection in both patients remains unknown.
Mycoplasma species lack a peptidoglycan cell wall and fail to show Gram reaction on Gram stain. Also, it is a slow-growing organism on the routinely used media in microbiology and appears as tiny pinpoint colonies. Special media SP4 broth, agar with arginine, or Shepard’s 10B broth is required to isolate the organism. M. hominis often grows on anaerobic media. Collectively, the unique characteristics of the organism pose a challenge to identifying the organism in a diagnostic laboratory. Therefore, molecular techniques are employed to successfully and promptly identify the organism more than the conventional methodologies [5–7].
M. hominis has a unique metabolism requirement. It lacks genes encoding for the pyruvate dehydrogenase complex, and the energy production is independent of the oxidation of pyruvate to acetyl-CoA. The presence of a gene encoding acetate kinase (ackA, MHO_3840) in M. hominis suggests its role in ATP production [8]. During energy generation, M. hominis utilizes arginine, which can potentially increase the ammonia level in the blood, and the unregulated ammonia levels result in serious complications such as Hyperammonemia syndrome (HS) [9]. Regardless of suspicion of liver disease, at the onset of neurological changes ammonia levels should be tested in transplant patients. Although the exact mechanism of hyperammonemia due to M. hominis is not clear, a non-glycolytic specie, M. hominis utilize arginine or hydrolyze urea for energy production, which might cause a subsequent increase in ammonia level as a byproduct resulting in brain edema and also necessitating continuous renal replacement therapy (CRRT) [10, 11].
Amongst several factors, adherence of M. hominis to the cell membrane results in colonization, and disseminated infection occurs due to the attachment to the mucosal epithelial cells[12]. Although exposure to M. hominis is self-limiting, the extragenital presence of M. hominis is associated with immunosuppressive status, and the organism has a propensity to appear in transplant patients [13]. The extragenital prevalence of the organism in transplant patients warrants genotypic profiling to understand the underlying mechanism of pathogenicity in transplant patients.
M. hominis is inherently resistant to macrolides. Due to the absence of a cell wall beta-lactams are ineffective against the organism. However, the organism is susceptible to clindamycin, doxycycline, and fluoroquinolone[6, 14]. In the cases presented, the diagnostic result of the donors before transplant were negative however, we cannot rule out the possibility of donor-derived infection in both cases as a small subset (1–3%) of healthy individuals harbors M. hominis in the respiratory secretions[15].
We present a rare occurrence of M. hominis infection in two transplant patients in which one patient developed right-side atelectasis and pulmonary insufficiency, and the other remained on CRRT post-transplant. M. hominis is a fastidious organism that can remain undetected for a longer duration. Its unique characteristics delay the diagnosis, which can cause significant morbidity post-transplantation. The incidence of M. hominis in solid organ transplants is under-recognized, and further studies can help alleviate the challenges associated with the prevention and treatment strategies for M. hominis infection in transplant patients.
We herein summarize (Table 1) 11 cases of M. hominis in lung and heart transplants from 2011 to 2021. Of the 11 patients, 7 males (64%) and 4 females (36%) with a mean age of 49 ( range 28–65 years) and 43 (range 18–64 years) were positive for M. hominis respectively. The mean duration from the onset of chief complaint post-transplantation and identification of M. hominis was 12 days (range 4–36 days). Ten cases (91%) utilized molecular techniques such as primer-specific PCR or 16 sRNA sequencing, and only 1 case (9%) used the identification of M. hominis solely based on the anaerobic culture growth method. The chief complaint in the 11 cases due to infection range from fever, pulmonary insufficiency, and right hip groin pain to severe encephalopathy. Two patients (18%) expired due to complications associated with M. hominis post-transplantation [4, 9, 15–22].
Table 1
shows the summary of 11 cases (2010–2021) of M. hominis in Lung and heart transplant patients.
| Authors and year | Age (yrs.) | Sex | Underlying condition | Transplant | Complaint after transplant | Treatment | Diagnosis method | POD- identification of M hominis (days) |
| Matteo Vecchio et al., 2021 | 56 years | M | Rapidly progressive pulmonary fibrosis | Bilateral Lung transplant | Fever, hypoxemia and pneumoniae | Doxycycline and oral moxifloxacin | Real-time quantitative PCR (qPCR) | 9 |
| Avika Dixit et al., 2017 | 18 year | F | Monosomy 7 and Myelodysplasia | Bilateral lung transplantation. | Chronic bronchitis with a mixed inflammatory infiltrate and variable mural fibrosis | Moxifloxacin and clindamycin | 16S ribosomal ribonucleic acid (rRNA) gene sequencing | 20 |
| D. Mitsani et al., 2010 | 64 years | M | Emphysema | Double lung transplantation | Respiratory failure | 6-week course of doxycycline | Anaerobic culture | 6 |
| Hideharu Hagiya et al., 2017 | 21 years | M | Restrictive cardiomyopathy and pulmonary hypertension | Heart–lung transplantation | Respiratory failure | Minocycline and levofloxacin | Direct colony polymerase chain reaction (PCR) using M. hominis-specific primers | 36 |
| Olivia C Smibert et al., 2017 | 65 years | F | Bronchiolitis obliterans secondary to seropositive rheumatoid arthritis | Bilateral sequential lung transplant | Respiratory failure with bilateral interstitial infiltrates | Moxifloxacin 400 mg daily and doxycycline 200 mg daily for 2 weeks | 16S rRNA sequencing | 19 |
| Olivia C Smibert et al., 2017 | 65 | M | Non–cystic fibrosis–related bronchiectasis | Bilateral lung transplant | Worsening respiratory function | 10 days of moxifloxacin | 16S rRNA sequencing | Not specified |
| Olivia C Smibert et al., 2017 | 51 | M | Cystic fibrosis–related bronchiectasis | Redo bilateral lung transplantation (chronic rejection) | Right hip and groin pain | Moxifloxacin and doxycycline | 16S rRNA sequencing | 29 |
| Mark Ewylam et al., 2013 | 64 years | F | Pulmonary fibrosis | Bilateral-sequential lung transplantation | Severe encephalopathy | patient expired | DNA sequencing | 4 |
| Charlotte Michel et al., 2021 | 55 years | M | Idiopathic pulmonary fibrosis | Double lung transplantation | Acute respiratory distress | azithromycin and doxycycline | specific PCR | 12 |
| Filippo Givone et al., 2020 | 28 years | M | Thoracic aortic aneurysm associated with aortic insufficiency | Orthotropic HT | High-grade fever, an aortic murmur without signs of heart failure | moxifloxacin 400 mg/day. | 16S ribosomal DNA PCR. | Not specified |
| Iva Kotaskova et al., 2017 | Young (age not specified) | F | Infective endocarditis | valve replacement | Fever and cough | Patient expired | PCR | Not specified |