A seventeen-year-old boy in New Delhi arrived at hospital with blistered, infected skin on both lower legs, sepsis, and kidneys failing so rapidly that he needed dialysis. He had been taking prednisolone for only a month to treat a newly diagnosed kidney scarring disease called focal segmental glomerulosclerosis. What clinicians found in his wounds turned out to be a bacterium so unusual, and so resistant to antibiotics, that it has rarely been documented in this setting: Myroides odoratus, a gram-negative bacillus that manufactures its own defense against most beta-lactam drugs. The case, published in BMC Infectious Diseases by a team at Maulana Azad Medical College, is the first reported instance of Myroides cellulitis occurring in a patient with nephrotic syndrome, according to the authors’ review of the literature.
The clinical picture was alarming from the outset. The adolescent presented with bullous cellulitis, meaning the infection had produced large fluid-filled blisters across the skin of both legs. Cellulitis itself is common, but this was no ordinary skin infection. Within days the boy developed sepsis, the body’s overwhelming inflammatory response to bloodstream-borne infection, and his kidneys deteriorated to stage 3 acute kidney injury under the Kidney Disease: Improving Global Outcomes classification, the most severe tier of that staging system. Hemodialysis was required to take over the work of filtering his blood while his kidneys recovered.
The immunological context matters enormously here. Focal segmental glomerulosclerosis is a disease in which scar tissue forms in parts of the glomeruli, the microscopic filters of the kidney, causing protein to leak into the urine and producing nephrotic syndrome. Standard treatment begins with corticosteroids such as prednisolone, which suppress the immune system to reduce inflammation in the kidney tissue. But that same immunosuppression leaves patients vulnerable to infections that healthy immune systems would normally repel with ease. The authors of the report emphasize that adolescents with nephrotic syndrome receiving corticosteroids are distinctly susceptible to severe polymicrobial soft-tissue infections, where multiple bacterial species invade the same wound simultaneously.
Treatment began empirically, as it often does when culture results take days to return. The boy was started on amoxicillin-clavulanate and clindamycin, a reasonable first-line combination for skin and soft-tissue infections. It failed. At forty-eight hours, clinicians escalated to piperacillin-tazobactam, a broader-spectrum beta-lactam combination, plus linezolid, which targets gram-positive organisms. The escalation reflected the severity of the sepsis and the failure of the initial regimen, but the true identity of the pathogens remained unknown until pus cultures came back on day four.
Those cultures revealed a polymicrobial growth: two organisms coexisting in the infected tissue. One was Klebsiella pneumoniae, a familiar and often drug-resistant hospital pathogen. The other was Myroides odoratus, a rare non-fermenting gram-negative bacillus that most clinicians will never encounter in their careers. The name derives from the distinctive odor the bacterium produces in culture, but its more alarming feature is its intrinsic resistance profile. Myroides species carry chromosome-encoded metallo-beta-lactamases, enzymes that dismantle the beta-lactam ring at the core of penicillins, cephalosporins, and carbapenems. This resistance is built into the bacterium’s genome rather than acquired on plasmids, meaning it is present even in isolates that have never seen an antibiotic.
Susceptibility testing delivered a sobering verdict: the Myroides isolate was susceptible only to minocycline, a tetracycline-class antibiotic. The clinicians therefore constructed a targeted regimen attacking both organisms at once, combining intravenous minocycline against the Myroides with ceftazidime, a third-generation cephalosporin active against the Klebsiella. The approach worked. The boy’s fever resolved by day ten, and by day twenty-five his kidneys had recovered sufficiently for dialysis to stop, with repeat cultures coming back sterile. The authors are careful to note, however, that because two pathogens were treated concurrently, Myroides odoratus cannot be regarded as the sole cause of the cellulitis, the sepsis, or the kidney injury, and the relative contribution of each organism cannot be distinguished.
More than one hundred human infections caused by Myroides species have been documented in the medical literature, but they remain concentrated in specific vulnerable populations: immunocompromised patients, those with indwelling devices, and people with extensive healthcare exposure. The organism has been implicated in ventilator-associated pneumonia, urinary tract infections, bacteremia, and wound infections, often with grim outcomes because of its resistance profile. Published evidence indicates that minocycline is among the agents most consistently active against Myroides, which is why the authors argue that susceptibility testing should guide therapy whenever this organism is isolated. Empirical regimens, they suggest, are largely futile against it.
The technical details of the case illuminate broader principles in infectious disease management. Early pus culture, obtained before antibiotic escalation obscures the microbial picture, proved decisive. Matrix-assisted laser desorption ionization time-of-flight mass spectrometry, the standard modern method for identifying bacteria by their protein fingerprints, and 16S ribosomal RNA sequencing, which reads the organism’s genetic barcode, are the tools typically deployed to confirm an unusual identification like Myroides. Minimum inhibitory concentration testing then determines which antibiotics actually work. Without these laboratory capabilities, the infection might have been treated blindly with progressively broader drugs, all of them defeated by the metallo-beta-lactamases, while the patient deteriorated.
For the nephrology community, the case is a reminder that corticosteroid therapy for glomerular disease creates a narrow window of vulnerability. Patients one month into prednisolone treatment are not yet in remission, their immune systems are already blunted, and their skin barriers may be compromised by edema, the fluid accumulation that accompanies nephrotic syndrome. Edematous skin stretches and weakens, creating entry points for bacteria. When cellulitis appears in such a patient, particularly bullous cellulitis involving both limbs, the threshold for aggressive investigation and broad-spectrum coverage should be low.
The authors conclude that the case illustrates both the danger and the solution: the vulnerability of immunosuppressed adolescents with kidney disease to severe polymicrobial soft-tissue infection, and the value of early culture with susceptibility-directed therapy when empirical regimens fail. The boy survived, his kidneys recovered, and the episode adds a rare data point to the clinical record of an organism that most physicians will encounter only in textbooks. As antimicrobial resistance continues to expand globally, cases like this one, in which a single susceptible antibiotic made the difference between recovery and disaster, underscore why microbiology laboratories remain the quiet backbone of modern medicine.
Subject of Research: Infectious Diseases
Article Title: Myroides odoratus polymicrobial cellulitis complicated by sepsis and acute kidney injury in an adolescent with focal segmental glomerulosclerosis: a case report
Article References: Kumar, S., Lodha, S. M., Acharya, S., & Garg, S. (2026). Myroides odoratus polymicrobial cellulitis complicated by sepsis and acute kidney injury in an adolescent with focal segmental glomerulosclerosis: a case report. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14676-7
Image Credits: AI Generated
DOI: 10.1186/s12879-026-14676-7
Keywords: Myroides odoratus, antimicrobial resistance, nephrotic syndrome, cellulitis, acute kidney injury, minocycline, Myroides, odoratus, polymicrobial, complicated, sepsis, acute
Cite Scienmag News
Jerry Hayes. (October 16, 2026). Rare Antibiotic-Resistant Bacterium Complicates Teen’s Kidney Disease Case. Scienmag. https://scienmag.com/rare-antibiotic-resistant-bacterium-complicates-teens-kidney-disease-case/
Jerry Hayes. "Rare Antibiotic-Resistant Bacterium Complicates Teen’s Kidney Disease Case." Scienmag, 16 October 2026, https://scienmag.com/rare-antibiotic-resistant-bacterium-complicates-teens-kidney-disease-case/. Accessed 16 October 2026.
Jerry Hayes. "Rare Antibiotic-Resistant Bacterium Complicates Teen’s Kidney Disease Case." Scienmag. October 16, 2026. https://scienmag.com/rare-antibiotic-resistant-bacterium-complicates-teens-kidney-disease-case/

