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Leuconostoc mesenteroides Bacteremia in a Patient With Lower Extremity Cellulitis

Authors:
Haowei Han, DO
Transitional Year Resident, Peconic Bay Medical Center–Northwell Health, Riverhead, New York

Sandeep A. Gandhi, MD
Infectious Diseases Consultant at Peconic Bay Medical Center–Northwell Health, Riverhead, New York, and Associate Professor of Clinical Medicine, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, New York

Kaushik Manthani, DO
Program Director, Transitional Year Residency Program, Peconic Bay Medical Center–Northwell Health, Riverhead, New York

Citation:
Han H, Gandhi SA, Manthani K. Leuconostoc mesenteroides bacteremia in a patient with lower extremity cellulitis [published online September 12, 2019]. Infectious Diseases Consultant.

 

A 51-year-old woman with a history of obesity, bilateral lower-extremity edema, type 1 diabetes mellitus, rheumatoid arthritis, multiple sclerosis, and spinal stenosis presented to the emergency department (ED) with left leg swelling, pain, redness, and abnormal warmth.

She had previously received a diagnosis of cellulitis and had been treated with amoxicillin clavulanate and cephalexin as an outpatient. She was not on any disease-modifying antirheumatic drugs (DMARDs) due to her having lost her health insurance coverage. Her medications were acidophilus-sporogenes, 1 tablet orally twice daily; cyclobenzaprine, 10 mg orally 3 times daily; gabapentin, 400 mg orally 3 times daily; hydralazine, 25 mg orally twice daily; insulin lispro subcutaneously 4 times daily before meals and at bedtime; lisinopril, 5 mg orally daily; and topical nystatin cream twice daily for a rash on her thigh and under her breasts. She also had been taking morphine extended release, 100 mg orally 3 times a day for more than 1 year.

Her vital signs were normal, and the results of a complete blood cell count (CBC) and basic metabolic panel were unremarkable, except for hyperglycemia. She was admitted to the hospital for recalcitrant cellulitis and was treated with intravenous (IV) piperacillin-tazobactam and linezolid.

Four days later, the patient developed new-onset diarrhea without fever, along with leukocytosis. Polymerase chain reaction stool tests results were positive for Clostridium difficile, and the colitis was treated with a 10-day course of oral vancomycin. She was discharged on oral linezolid for an additional 3 days.

Three weeks later, the patient was readmitted to the ED due to recurrent cellulitis. At this presentation, she denied having any other associated symptoms, a history of recent travel, dental work, or zoonotic exposures. Her vital signs were stable, and her leukocyte count was within normal limits. Her erythrocyte sedimentation rate was noted to be elevated at 41 mm/h. Laboratory test results were significant for a white blood cell count of 6000/µL, neutrophils of 3700/µL, and a hemoglobin level of 10.5 g/dL. Blood cultures were drawn, and she was treated with oral doxycycline and discharged. However, 1 of 4 blood cultures grew gram-positive cocci in an anaerobic blood culture 2 days later.

The patient was readmitted to the hospital for treatment of bacteremia with IV vancomycin and piperacillin-tazobactam. Her vital signs and CBC results were normal. The patient said that she had been feeling better, and the cellulitis had improved after outpatient antibiotic treatment. Three days later, the infectious agent was identified as Leuconostoc mesenteroides.

She was then started on IV ampicillin and gentamicin. However, the gentamicin caused intolerable nausea and subjective fevers after the second infusion. Therefore, gentamicin was switched to ceftriaxone, 2 g/d IV. After 7 days of this treatment, the patient felt better, the cellulitis had resolved, and she had had no further fevers; she was discharged home with a peripherally inserted central catheter to finish a total of a 14-day course of antibiotics. The bacterium was sensitive to ampicillin, chloramphenicol, penicillin, and minocycline and had an intermediate sensitivity to gentamicin and ceftriaxone.

NEXT: Discussion

DISCUSSION

Species of the Leuconostoc genus are gram-positive, catalase-negative, microaerophilic cocci.1 Rarely, they can be found in gastric or vaginal fluids, but they are not considered to be part of normal human flora.2 Due to some shared biological features, Leuconostoc species might be misidentified as Lactobacillus, Streptococcus (particularly the viridans group), Pediococcus, or Enterococcus.3 The bacteria also play a role in the fermentation of milk, wine, and pickles.4

Clinically, Leuconostoc species are characterized by their intrinsic resistance to vancomycin due to a lack of a target in the cell wall.5 Nevertheless, the recommended antibiotic treatment includes penicillin G, ampicillin, clindamycin, carbapenems, and aminoglycosides.5 Successful treatment with tigecycline has also been reported.6

Cases of infection with Leuconostoc species are rarely reported. Risk factors for infection with Leuconostoc species include immunosuppressed states, central venous line insertion, and recent vancomycin therapy. For example, a case was reported of L mesenteroides meningitis associated with HIV and central nervous system tuberculosis.7 However, L mesenteroides has also been described in several immunocompetent patients, including empyema in a healthy man producing and selling sauerkraut and pickled vegetables.4 One group of authors reported a case of endophthalmitis in a healthy man after phacoemulsification and posterior chamber implantation.1

In one instance, Leuconostoc lactis bacteremia was diagnosed in a patient with gastrointestinal (GI) tract amyloidosis secondary to rheumatoid arthritis and tuberculous arthritis.8 L mesenteroides bacteremia was also reported in a patient with partial gastrectomy secondary to Chagas disease.9

Regarding the route of infection, many authors speculate that disruption of the GI barrier may be a risk factor for Leuconostoc bacteremia, given that it is more commonly seen in neonates with short bowel syndrome.2,7 Additionally, some authors have suggested the skin to be a possible source for this pathogen, since several cases have been diagnosed after central venous catheter insertion or the initiation of total parenteral nutrition (TPN).9,10 In the largest nosocomial outbreak reported so far, 40 of 42 patients with Leuconostoc bacteremia were on TPN.10 Nevertheless, there is no well-established theory regarding the route of infection.

In our patient’s case, the primary risk factor was chronic immunosuppression. Other risk factors included type 1 diabetes mellitus, a chronic inflammatory condition that alters the duodenal mucosa microbiome,11 and that the patient was on long-term opioids, which also can disrupt the GI flora.12 However, because L mesenteroides is not part of the normal flora, the impact of diabetes and chronic opiate use in its pathogenesis needs more epidemiological study.

We suspect that the pathogenesis in this case was cellulitis, which resulted in microscopic skin breaks and chronic edema induced by venous stasis, leading to the development of bacteremia. Another possibility is that the GI barrier was disrupted by her chronic autoimmune disease, leading to bacteremia. Vancomycin may have played a role in the growth of L mesenteroides.

In conclusion, Leuconostoc bacteremia should be suspected in a patient with immunosuppression, prolonged use of vancomycin, skin trauma, and/or GI tract pathology. Because of the widespread use of vancomycin, Leuconostoc infection may be a cause for increasing concern in the infectious diseases specialty.

REFERENCES:

  1. Kumudhan D, Mars S. Leuconostoc mesenteroides as a cause of post-operative endophthalmitis—a case report. Eye (Lond). 2004;18(10):1023-1024.
  2. Karbuz A, Kocabaş BA, Yalman A, et al. Catheter related Leuconostoc mesenteroides bacteremia: a rare case and review of the literature. J Pediatr Res. 2017;4(1):35-38.
  3. Cappelli EA, Barros RR, Camello TCF, Teixeira LM, Merquior VLC. Leuconostoc pseudomesenteroides as a cause of nosocomial urinary tract infections. J Clin Microbiol. 1999;37(12):4124-4126.
  4. Usta-Atmaca H, Akbas F, Karagoz Y, Piskinpasa ME. A rarely seen cause for empyema: Leuconostoc mesenteroides. J Infect Dev Ctries. 2015;9(4):425-427.
  5. Ino K, Nakase K, Suzuki K, Nakamura A, Fujieda A, Katayama N. Bacteremia due to Leuconostoc pseudomesenteroides in a patient with acute lymphoblastic leukemia: case report and review of the literature. Case Rep Hematol. 2016;2016:7648628.
  6. Patel T, Molloy A, Smith R, Balakrishnan I. Successful treatment of Leuconostoc bacteremia in a neutropenic patient with tigecycline. Infect Dis Rep. 2012;4(2):e31.
  7. Barletta J, Estrada T, Rolón MJ, Erbin M, Kauffman S, Pérez H. Meningitis due to Leuconostoc mesenteroides associated with central nervous system tuberculosis: a case report. Ann Clin Case Rep. 2017;2:1228.
  8. Shin J, Her M, Moon C, Kim D, Lee S, Jung S. Leuconostoc bacteremia in a patient with amyloidosis secondary to rheumatoid arthritis and tuberculosis arthritis. Mod Rheumatol. 2011;21(6):691-695.
  9. Menegueti MG, Gaspar GG, Laus AM, Basile-Filho A, Bellissimo-Rodrigues F, Auxiliadora-Martins M. Bacteremia by Leuconostoc mesenteroides in an immunocompetent patient with chronic Chagas disease: a case report. BMC Infect Dis. 2018;18(1):547.
  10. Bou G, Saleta JL, Nieto JAS, et al. Nosocomial outbreaks caused by Leuconostoc mesenteroides subsp. mesenteroides. Emerg Infect Dis. 2008;14(6):968-971.
  11. Pelligrini S, Sordi V, Bolla AM, et al. Duodenal mucosa of patients with type 1 diabetes shows distinctive inflammatory profile and microbiota. J Clin Endocrinol Metab. 2017;102(5):1468-1477.
  12. Banerjee S, Sindberg G, Wang F, et al. Opioid-induced gut microbial disruption and bile dysregulation leads to gut barrier compromise and sustained systemic inflammation. Mucosal Immunol. 2016;9(6):1418-1428.