Volume 29, Number 3—March 2023
Inquilinus limosus Bacteremia in Lung Transplant Recipient after SARS-CoV-2 Infection
Inquilinus limosus is an environmental bacterium associated with respiratory tract colonization in cystic fibrosis patients. We report a case of I. limosus bacteremia in a patient in France who received a lung transplant and experienced chronic graft dysfunction and SARS-CoV-2 infection. This case suggests I. limosus displays virulence factors associated with invasion.
A 45-year-old woman in France who had received a lung transplant in 2016 for end-stage cystic fibrosis (CF) sought care for rhinorrhea on March 1, 2022. Her immunosuppressive regimen included mycophenolate mofetil (750 mg 2×/d) and cyclosporine A (200 mg 2×/d). She received oral azithromycin (250 mg/d) and trimethoprim/sulfamethoxazole 400 (80 mg/d) for pneumocystosis prophylaxis. In 2021, she experienced progressive graft dysfunction with no obvious trigger and was treated with alemtuzumab in June 2021. Her forced expiratory volume decreased from 78% in January 2021 to 57% in May 2021 and 30% in January 2022.
At the visit, the patient tested positive for SARS-CoV-2 by reverse transcription PCR. She returned home with treatment for symptoms; she had a productive cough with greenish sputum, for which she received 7 days of amoxicillin/clavulanate. Because her condition did not improve, she continued the treatment for 14 more days. On April 11, we isolated a strain of P. aeruginosa (106 CFU/mL) from her sputum and prescribed cefepime (2 g/d). However, her condition worsened, and she was hospitalized on April 20. A chest computed tomography showed bilateral nodular condensations in the lungs; we switched cefepime for piperacillin/tazobactam and tobramycin. Several respiratory samples grew Inquilinus limosus and Pseudomonas aeruginosa (Table). We recovered A. fumigatus from bronchoalveolar liquid and started the patient on posaconasole (300 mg/d). No mycobacteria were recovered.
An aerobic vial of a blood culture set sampled on April 26 was positive for I. limosus after 87 hours of incubation. We identified I. limosus using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry after subculture and formic acid extraction. We replaced the treatment with ceftolozane/tazobactam. We determined MIC as follows: piperacillin/tazobactam, >32 mg/L; cefepime, 256 mg/L; ceftolozane/tazobactam, 256 mg/L; imipenem, 0.047 mg/L; meropenem, 0.012 mg/L; and ciprofloxacin, 0.016 mg/L. Ceftolozane/tazobactam was switched for meropenem plus amikacin and then ciprofloxacin on May 4. The patient improved but remained colonized with I. limosus, displaying a similar pattern of resistance, 3 months later. Of interest, she was colonized before the lung transplantation, but I. limosus has not been isolated since then.
I. limosus is a fastidious, gram-negative rod from environmental sources (1) that has rarely been associated with colonization of the respiratory tract of CF patients (2). The airways of CF are susceptible to colonization by respiratory pathogens (3), a condition that is improved in lung transplant recipients. Nevertheless, I. limosus infection has been reported twice in lung transplant recipients (4,5). In 1 case, a 22 year-old woman had pulmonary infiltrates develop within a month after lung transplantation (4). She completely recovered with antimicrobial drug treatment; I. limosus was not isolated during 1 year of follow-up. In the second case, a 31-year-old man experienced a bacteremic lung empyema 1 month posttransplant and a contralateral lung empyema 7 months later (5). He recovered from each episode with surgery and antimicrobial treatment with ciprofloxacin and meropenem. Both patients were lung transplant recipients for end-stage cystic fibrosis (CF); they were colonized with I. limosus before lung transplantation. Indeed, the lung graft microbiome is affected by donor and recipient factors (6), but early posttransplant infections mainly involve the bacteria of the recipient rather than those of the donor (7).
In contrast to those patients, the case-patient we describe experienced a late infection several years after I. limosus clearance. Unfortunately, the pretransplant strain was not preserved, and we could not determine whether she was infected with the strain she was colonized with before the lung transplantation or another strain. It is possible that the chronic graft dysfunction, the recent intensification of immunosuppression, and the SARS-CoV-2 infection could have led to a modification of the graft microbiome and enabled colonization with I. limosus. In CF patients, colonization with I. limosus induces a specific serum antibody response (8). The intensification of immunosuppression and the clearance of I. limosus after lung transplantation could have reduced humoral immunity. Furthermore, the bacteremia suggested virulence factors involved in the invasion. Two other cases of I. limosus bacteremia have been reported previously (5,9).
Because I. limosus is a rarely encountered microorganism and because its colonies are of a mucoid morphotype, it could be misidentified using phenotypic characteristics as P. aeruginosa (8,10). The biochemical methods used previously provided inconsistent identification, and neither European Committee on Antimicrobial Susceptibility Testing nor Clinical and Laboratory Standards Institutes guidelines include standardized I. limosus antimicrobial susceptibility testing. However, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry accurately identifies I. limosus. I. limosus displays high MICs for colistin and almost all β-lactams, except imipenem and meropenem (9). It has been suggested that the multidrug resistance of I. limosus enhances its selection in CF patients (2). In our case, successive treatment with drugs that were ineffective against I. limosus could have enabled its selection.
In conclusion, we emphasize a pathogenic role of I. limosus in lung transplant recipients several years after respiratory clearance of the bacteria. Chronic graft dysfunction, intensifying immunosuppression, and SARS-CoV-2 infection in this patient could have favored colonization with I. limosus. Characteristics of the bacterium such as colony morphotypes and multidrug resistance could delay effective therapy.
Dr. Farfour is a medical microbiologist at Foch Hospital clinical laboratory, Suresnes, France. His primary research interests are emerging pathogens and antimicrobial drug resistance.
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TableCite This Article
Original Publication Date: February 15, 2023
Table of Contents – Volume 29, Number 3—March 2023
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Please use the form below to submit correspondence to the authors or contact them at the following address:
Eric Farfour, Service de biologie Clinique, Hôpital Foch, 40 rue Worth, 92150 Suresnes, France