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Esophageal erosion as a possible bacterial entry site in an acute lymphoblastic leukemia patient with sepsis

Satoshi Ikegaya1, Akira Yoshida, Hiromichi Iwasaki

  • 1Second Department of Pathology, Fukui Medical University, Yoshida-gun, Fukui, Japan.

International Journal of Hematology
|May 31, 2003
PubMed

Insights

This case study highlights a fatal Enterococcus faecalis infection in a leukemia patient undergoing chemotherapy. Esophageal erosions, linked to herpes simplex virus, were identified as the likely entry point for the bacteria, clarifying infection pathogenesis.

Area of Science:

  • Oncology
  • Infectious Diseases
  • Pathology

Background:

  • Acute lymphoid leukemia (ALL) patients undergoing chemotherapy are immunocompromised.
  • Febrile neutropenia is a common and serious complication in these patients.
  • The precise origin of infections in febrile neutropenia is often unclear.

Observation:

  • A 69-year-old man with relapsed ALL developed sepsis and meningitis during chemotherapy (adriamycin, vincristine, prednisolone).
  • Despite broad-spectrum antimicrobials (imipenem, meropenem, amphotericin-B, gamma-globulin), the patient succumbed to respiratory failure.
  • Blood and cerebrospinal fluid cultures were positive for Enterococcus faecalis.

Findings:

  • Autopsy revealed esophageal erosions with herpes simplex virus (HSV) nuclear inclusion bodies.
  • Micrococci proliferation was noted at erosion bases and in submucosal vessels.
  • These findings suggest E. faecalis translocation from esophageal lesions into the bloodstream.

Implications:

  • This case provides a potential explanation for the source of E. faecalis bacteremia in febrile neutropenia.
  • Understanding the pathogenesis of infection in immunocompromised patients is crucial for improving outcomes.
  • The interplay between HSV, micrococci, and E. faecalis in esophageal lesions warrants further investigation.

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