Microbacterium resistens Peritoneal Dialysis–Associated Peritonitis: A Case Report

Abstract

Peritoneal dialysis (PD)–associated peritonitis is most commonly caused by Gram-positive organisms; however, infections due to unusual pathogens can present important diagnostic and management challenges. Microbacterium resistens is an environmental Gram-positive bacillus rarely implicated in human infections, and PD-associated peritonitis due to this organism has been reported only once previously, to our knowledge. We report a case of persistent PD-associated peritonitis caused by M resistens in a 65-year-old man receiving automated PD combined with once-weekly hemodialysis. The initial episode was treated by prioritizing the already identified Enterococcus casseliflavus; an initially unidentified Gram-positive bacillus was subsequently identified as M resistens. The patient experienced multiple subsequent episodes despite sequential systemic and intraperitoneal antimicrobial therapies. Although effluent leukocyte counts repeatedly normalized with treatment, M resistens was repeatedly isolated with unchanged antimicrobial susceptibility profiles, suggesting persistent catheter colonization rather than acquired antimicrobial resistance. A definitive cure was achieved only after PD catheter removal. This case highlights that apparent clinical response with effluent leukocyte normalization does not necessarily indicate microbiological eradication in rare device-associated infections and that early catheter removal should be considered when the same unusual organism is repeatedly isolated despite appropriate antimicrobial therapy.

Peritoneal dialysis (PD)–associated peritonitis remains a major complication that affects patient outcomes and technique survival.¹ Although most episodes are caused by common Gram-positive organisms, infections due to unusual pathogens can present important diagnostic and therapeutic challenges, particularly when they involve indwelling devices.² Among these organisms, Microbacterium species are environmental aerobic Gram-positive bacilli and infrequent human pathogens3, 4, 5 but have been implicated in catheter-related infections.⁶ Reports specifically involving PD-associated peritonitis due to Microbacterium resistens are exceedingly rare, with only one prior case identified in the literature.⁷ Available reports suggest that infections caused by Microbacterium species may be difficult to eradicate and can be associated with recurrent infection and catheter removal.^3,5,7 However, the clinical course and optimal management remain poorly defined. Here, we report a case of M resistens PD-associated peritonitis with multiple subsequent episodes despite sequential systemic and intraperitoneal antimicrobial therapies, ultimately requiring PD catheter removal. This case highlights that apparent clinical improvement with effluent leukocyte normalization does not necessarily indicate microbiological eradication in device-associated infections.

Case Report

A 65-year-old man with end-stage kidney disease due to IgA nephropathy initiated hemodialysis in 2023 and transitioned to combined automated PD with once-weekly hemodialysis in January 2025 for occupational reasons. His clinical course was stable, and no episodes of PD-associated peritonitis occurred during the first 10 months after PD initiation.

On October 18, 2025, he developed abdominal pain followed by cloudy peritoneal effluent. He was admitted on October 21 with suspected PD-associated peritonitis. Analysis of peritoneal effluent revealed a leukocyte count of 1,950 cells/μL with neutrophil predominance. Automated PD was discontinued, and the patient was temporarily managed with hemodialysis 3 times weekly. Empiric intravenous cefazolin and ceftazidime were initiated in accordance with institutional practice. No exit-site or tunnel infection was observed. Cultures of peritoneal effluent grew Enterococcus casseliflavus and an aerobic Gram-positive bacillus. Because species identification of E casseliflavus became available earlier, antimicrobial therapy was narrowed to intravenous ampicillin/sulbactam while definitive identification of the Gram-positive bacillus was pending. The effluent cleared, and leukocyte counts decreased to <20 cells/μL. Automated PD was resumed, and the patient was discharged with oral levofloxacin.

After discharge, the previously unidentified Gram-positive bacillus was identified as M resistens. The patient’s PD technique and possible environmental exposures were then reviewed. No apparent break in aseptic PD technique was identified, and there was no exit-site or tunnel infection. The patient did not report regular exposure to soil, wastewater, gardening, livestock, or other obvious environmental sources at home or work. Therefore, although M resistens is considered an environmental organism, no definite source of acquisition could be identified. While still receiving oral levofloxacin, the patient developed recurrent abdominal pain and cloudy effluent on November 3. Effluent leukocyte count was 797 cells/μL, consistent with a subsequent episode of PD-associated peritonitis. Cultures again grew M resistens. Based on antimicrobial susceptibility testing, antibiotic therapy was changed to high-dose intravenous ampicillin combined with oral azithromycin. Effluent leukocyte counts again decreased to <20 cells/μL with symptomatic improvement. However, additional episodes occurred despite ongoing systemic therapy. Because of the difficult-to-control clinical course, an infection control team was consulted, and treatment was changed to a combination strategy consisting of intraperitoneal ampicillin and ceftazidime combined with oral azithromycin. Effluent leukocyte counts again decreased to <20 cells/μL. However, several weeks after completion of therapy, peritonitis recurred with an effluent leukocyte count of 1,183 cells/μL, and cultures again grew M resistens. Intraperitoneal antibiotic therapy was reinitiated, but effluent leukocyte counts continued to increase to 2,275 cells/μL, indicating failure of effluent clearing. Abdominal computed tomography showed no intra-abdominal abscess, localized fluid collection, or other surgically treatable focus. The PD catheter was removed on January 5. The patient received intravenous ampicillin and ceftazidime for an additional 2 weeks, after which symptoms resolved and inflammatory markers normalized. He remained on maintenance hemodialysis thereafter.

Across all episodes, antimicrobial susceptibility profiles remained unchanged, suggesting persistent catheter colonization rather than acquired resistance. The overall clinical timeline is shown in Fig 1, and a detailed episode-by-episode summary, including effluent white blood cell counts, polymorphonuclear leukocyte percentages, culture results, and antimicrobial therapy, is provided in Table 1.

Figure 1.

Clinical timeline of PD-associated peritonitis caused by Microbacterium resistens. The patient experienced multiple subsequent episodes despite sequential systemic and IP antibiotic therapies. Definitive resolution was achieved only after PD catheter removal. Black arrow indicates initial episode of peritonitis, and red arrow indicates PD catheter removal. Abbreviations: ABPC, ampicillin; AZM, azithromycin; CAZ, ceftazidime; CEZ, cefazolin; CRP, C-reactive protein; IP, intraperitoneal; IV, intravenous; LVFX, levofloxacin; PD, peritoneal dialysis; PO, per os (oral administration); SBT, sulbactam; WBC, white blood cell.

Table 1.

Detailed Clinical Timeline of Recurrent Microbacterium resistens Peritoneal Dialysis–Associated Peritonitis

Day From Initial Admission	Date	Clinical Event	Effluent WBC, Cells/μL (PMN, %)	Culture Result	Antibiotic Therapy
Day 2	Oct 18	Onset of abdominal pain followed by cloudy peritoneal effluent	N/A	Not obtained	None
Day 1	Oct 21	Initial admission with abdominal pain and cloudy effluent	1,950 (80%)	Enterococcus casseliflavus and aerobic Gram-positive bacillus	IV CEZ + IV CAZ, then IV ABPC/SBT
Day 3	Oct 23	Improvement in effluent leukocyte count	200 (16%)	Pending identification	IV ABPC/SBT
Day 10	Oct 30	Discharge after clinical improvement	<20 (N/A)	Aerobic Gram-positive bacillus later identified as M resistens	Oral LVFX
Day 14	Nov 3	Recurrent abdominal pain and cloudy effluent while receiving oral LVFX	797 (N/A)	Culture result pending	IV CEZ + IV CAZ
Day 16	Nov 5	Persistent peritonitis	950 (41%)	M resistens	High-dose IV ABPC + oral AZM
Day 18	Nov 7	Improvement after antimicrobial change	202 (10%)	M resistens	High-dose IV ABPC + oral AZM
Day 24	Nov 13	Effluent leukocyte count normalized	<20 (N/A)	M resistens	High-dose IV ABPC + oral AZM
Day 31	Nov 20	Cloudy effluent again; antibiotics changed to the IP route	700 (73%)	Culture result pending	IP ABPC + IP CAZ + oral AZM
Day 33	Nov 22	Persistent peritonitis	439 (N/A)	M resistens	IP ABPC + IP CAZ + oral AZM
Day 36	Nov 25	Improvement in effluent leukocyte count	64 (15)	M resistens	IP ABPC + IP CAZ + oral AZM
Day 43	Dec 2	Continued IP antibiotics after discharge	<20 (N/A)	M resistens	IP ABPC + IP CAZ + oral AZM
Day 70	Dec 29	Recurrent abdominal pain and cloudy effluent	1,183 (N/A)	Culture result pending	IV CEZ + IV CAZ
Day 71	Dec 30	Antibiotics changed to the IP route	N/A	Culture result pending	IP ABPC + IP CAZ
Day 74	Jan 2	Persistent infection despite IP antimicrobial therapy	249 (N/A)	M resistens	IP ABPC + IP CAZ
Day 77	Jan 5	PD catheter removal because of failure of effluent clearing	2,275 (18%)	M resistens	IV ABPC + IV CAZ for 2 weeks

Abbreviations: ABPC, ampicillin; AZM, azithromycin; CAZ, ceftazidime; CEZ, cefazolin; IP, intraperitoneal; IV, intravenous; LVFX, levofloxacin; N/A, not available; PD, peritoneal dialysis; PMN, polymorphonuclear leukocytes; SBT, sulbactam; WBC, white blood cell.

Discussion

We report a rare case of PD-associated peritonitis caused by M resistens characterized by multiple subsequent episodes despite sequential antimicrobial therapy. A definitive cure was achieved only after PD catheter removal. As in the only previously reported case of PD-associated peritonitis due to M resistens, catheter removal was ultimately required for cure.

PD-associated peritonitis caused by Microbacterium species has been reported only sporadically in the literature. Most reported cases involve Microbacterium paraoxydans or other environmental species, whereas infection caused by M resistens is exceptionally rare.3, 4, 5^,7 To our knowledge, only 1 prior case of PD-associated peritonitis caused by M resistens has been described (Table 2).⁷ The extreme rarity of this organism in PD-associated infection limits available clinical experience and makes optimal management strategies difficult to establish.

Table 2.

Reported Cases of Peritoneal Dialysis–Associated Peritonitis Caused by Microbacterium resistens

Characteristic	Previously Reported Case7	Present Case
Age/sex	71 y/male	65 y/male
Primary kidney disease	Not reported	IgA nephropathy
Dialysis modality	Continuous ambulatory PD	Combined APD and once-weekly HD
PD duration	13 mo	10 mo
Initial presentation	Abdominal pain, cloudy effluent	Abdominal pain, cloudy effluent
Effluent WBC at presentation	3,990 cells/μL (neutrophil predominant)	1,950 cells/μL (neutrophil predominant)
Initial empirical therapy	IP cefazolin, and IP ceftazidime	IV cefazolin, and IV ceftazidime
Response to empirical therapy	Transient improvement	Transient improvement
Pathogen	M resistens	M resistens
Identification method	MALDI-TOF MS	MALDI-TOF MS
Antimicrobial susceptibility (MIC, mg/L)
Ampicillin	0.25	0.5
Cefazolin	32	N/A
Cefotaxime	12	>4
Ceftazidime	≥256	N/A
Erythromycin	12	≤0.12
Azithromycin	N/A	≤0.25
Vancomycin	16	>1
Rifampin	1	4
Levofloxacin	N/A	4
Duration from treatment initiation to catheter removal	∼4 mo	∼2.5 mo
PD catheter removal	Yes	Yes
Outcome after catheter removal	Cure	Cure

Abbreviations: APD, automated peritoneal dialysis; HD, hemodialysis; IP, intraperitoneal; IV, intravenous; MALDI-TOF MS, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry; MIC, minimum inhibitory concentration; N/A, not available; PD, peritoneal dialysis; PO, per os (oral administration); WBC, white blood cell.

The present case also illustrates an important diagnostic point. Although the initial episode was treated by prioritizing the already identified E casseliflavus, the initially unidentified Gram-positive bacillus was later identified as M resistens, and this organism was repeatedly isolated in subsequent episodes. These findings suggest that M resistens was the persistent pathogen driving the prolonged clinical course, even though the initial presentation suggested polymicrobial peritonitis.

Our case demonstrates a particularly challenging clinical course, with multiple subsequent episodes despite transient normalization of effluent leukocyte counts after both systemic and intraperitoneal antibiotic therapy. These findings suggest that short-term clinical improvement does not necessarily indicate microbiological eradication, particularly when device-associated pathogens are involved. In retrospect, earlier intraperitoneal ampicillin may have been reasonable, given the isolate’s susceptibility profile and the general preference for intraperitoneal antibiotics in PD-associated peritonitis. Initial intravenous therapy was selected because PD was temporarily interrupted during the acute phase. Intraperitoneal ampicillin-based therapy was subsequently introduced after repeated isolation of M resistens; however, recurrence still occurred, and effluent clearing eventually failed. This sequence suggests that antimicrobial delivery alone was insufficient once persistent catheter-associated colonization had been established.

Repeated isolation of M resistens with unchanged antimicrobial susceptibility profiles is most consistent with persistent colonization of the PD catheter, likely mediated by biofilm formation. Although the mechanisms of biofilm formation by M resistens remain poorly characterized, Microbacterium species are environmental Gram-positive, non–spore-forming bacilli that can persist in nutrient-limited environments and adhere to abiotic surfaces. Although specific adhesion factors of M resistens have not been defined, biofilm-forming ability has been described in other species of this genus.⁸ These observations support the plausibility of catheter-associated persistence in the present case. Biofilm-associated infections are well recognized in indwelling devices, where antibiotics may suppress planktonic organisms without eliminating bacteria embedded within the biofilm.^9,10 Thus, antimicrobial therapy may suppress planktonic organisms and lead to transient normalization of effluent leukocyte counts without eradicating bacteria embedded within catheter-associated biofilm. This mechanism may explain the discordance between apparent clinical response and repeated subsequent isolation of M resistens in our case. Microbiological or microscopic confirmation of biofilm formation on the removed catheter was not available, and the proposed mechanism therefore remains inferential. Nevertheless, repeated isolation of the same organism with unchanged antimicrobial susceptibility profiles strongly supports persistent catheter colonization rather than acquired antimicrobial resistance.

Although Microbacterium species are taxonomically distinct from nontuberculous mycobacteria, comparison with nontuberculous mycobacteria peritonitis is clinically informative. Both Microbacterium species and nontuberculous mycobacteria are environmental organisms that may be difficult to eradicate in the presence of an indwelling PD catheter. In addition, both can present with an initially nonspecific clinical course and may require prolonged microbiological evaluation for definitive organism identification. However, unlike nontuberculous mycobacteria peritonitis, for which the International Society for Peritoneal Dialysis guidelines include organism-specific recommendations and generally emphasize prolonged multidrug therapy and catheter removal in many cases, there are no established treatment recommendations for M resistens PD-associated peritonitis.^2,11 Therefore, management must be individualized according to clinical response, antimicrobial susceptibility profiles, repeated culture results, and evidence of persistent catheter-associated infection. In the present case, repeated isolation of M resistens with unchanged susceptibility profiles, recurrence despite systemic and intraperitoneal antimicrobial therapy, and eventual failure of effluent clearing supported PD catheter removal for definitive source control.

Current International Society for PD guidelines define refractory peritonitis primarily as failure of effluent clearing after 5 days of appropriate antibiotic treatment and recommend catheter removal for relapsing, recurrent, or repeat peritonitis.² Our case highlights a related clinical scenario in which effluent leukocyte counts initially normalize, but the same unusual organism is repeatedly isolated thereafter, suggesting persistent device-associated infection. These observations emphasize that apparent effluent response should not always be interpreted as a definitive cure when uncommon pathogens are isolated. In such situations, earlier catheter removal may help prevent repeated episodes and prolonged treatment courses.

In conclusion, M resistens is a rare but potentially difficult-to-eradicate cause of PD-associated peritonitis. Repeated isolation of the same organism despite apparent clinical improvement and stable antimicrobial susceptibility profiles may indicate persistent catheter colonization, and early consideration of PD catheter removal may be necessary to achieve a definitive cure.