3 Key Takeaways
Plain English Summary- 01Core Finding
Although LCMV is a rodent zoonosis with a global distribution, no UK cases in humans have been reported in published literature since the 1950s, and testing is rarely performed.
- 02Study Evidence
Tested in a in vivo animal model (preclinical discovery) at the preclinical stage.
- 03Practical Meaning
Antiviral therapy continued for 6 months.
What This Means for You
Molnupiravir was later substituted for favipiravir, and favipiravir dosing was guided by serum and CSF therapeutic drug monitoring. The patient showed sustained neurological improvement, with clearance of LCMV from CSF and blood within 2 months. Antiviral therapy continued for 6 months. The patient regained functional independence and returned to work, with only mild residual symptoms. In addition to reporting a novel occurrence of LCMV infection in a patient on teclistamab, the case highlights the presence of LCMV in the UK and the utility of metagenomic next-generation sequencing for pathogen identification in undiagnosed encephalitis. Finally, the case provides preliminary evidence supporting combination antiviral therapy in persistent LCMV infection.
The Discovery
Lymphocytic choriomeningitis virus (LCMV) is a rare cause of meningoencephalitis in humans. Although LCMV is a rodent zoonosis with a global distribution, no UK cases in humans have been reported in published literature since the 1950s, and testing is rarely performed. LCMV meningoencephalitis is self-limiting in people who are immunocompetent, but infection in hosts who are immunocompromised causes severe disease. We report a presentation of LCMV meningoencephalitis in a patient with relapsed multiple myeloma receiving teclistamab. The patient presented with a 5-month history of progressive neurological symptoms, including hearing loss, ataxia, headache, and weight loss. Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis, markedly elevated protein concentration, and hypoglycorrhachia. Extensive microbiological and autoimmune investigations were negative, and empirical antimicrobial and antituberculosis therapies did not prevent clinical deterioration. Metagenomic next-generation sequencing of CSF identified LCMV, and a history of domestic rodent exposure was subsequently identified. Combination antiviral therapy with ribavirin, remdesivir, and molnupiravir was initiated. Molnupiravir was later substituted for favipiravir, and favipiravir dosing was guided by serum and CSF therapeutic drug monitoring.
How It Works, Simply
This infectious disease research focuses on antibodies · Immune response. Researchers evaluated it using an in vivo animal model (Preclinical discovery) at the preclinical stage of medical research.
3 Key Takeaways
Clinical Takeaways- 01Core Finding
Although LCMV is a rodent zoonosis with a global distribution, no UK cases in humans have been reported in published literature since the 1950s, and testing is rarely performed.
- 02Study Evidence
Tested in a in vivo animal model (preclinical discovery) at the preclinical stage.
- 03Practical Meaning
Antiviral therapy continued for 6 months.
Key Numbers
Biological Mechanism & Study Design
Study Design & Cohort
Animal models
In vivo animal model (Preclinical discovery) · Preclinical
Biological Pathway & Modality
Antibodies · Immune response
Intervention: Combination antiviral treatment for a patient with lymphocytic choriomeningitis
Experimental Findings & Endpoints
Lymphocytic choriomeningitis virus (LCMV) is a rare cause of meningoencephalitis in humans.
Although LCMV is a rodent zoonosis with a global distribution, no UK cases in humans have been reported in published literature since the 1950s, and testing is rarely performed. LCMV meningoencephalitis is self-limiting in people who are immunocompetent, but infection in hosts who are immunocompromised causes severe disease.
We report a presentation of LCMV meningoencephalitis in a patient with relapsed multiple myeloma receiving teclistamab. The patient presented with a 5-month history of progressive neurological symptoms, including hearing loss, ataxia, headache, and weight loss.
Cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis, markedly elevated protein concentration, and hypoglycorrhachia. Extensive microbiological and autoimmune investigations were negative, and empirical antimicrobial and antituberculosis therapies did not prevent clinical deterioration.
Metagenomic next-generation sequencing of CSF identified LCMV, and a history of domestic rodent exposure was subsequently identified. Combination antiviral therapy with ribavirin, remdesivir, and molnupiravir was initiated.
Molnupiravir was later substituted for favipiravir, and favipiravir dosing was guided by serum and CSF therapeutic drug monitoring.
Clinical Translation & Practice Context
Molnupiravir was later substituted for favipiravir, and favipiravir dosing was guided by serum and CSF therapeutic drug monitoring.
The patient showed sustained neurological improvement, with clearance of LCMV from CSF and blood within 2 months. Antiviral therapy continued for 6 months.
The patient regained functional independence and returned to work, with only mild residual symptoms. In addition to reporting a novel occurrence of LCMV infection in a patient on teclistamab, the case highlights the presence of LCMV in the UK and the utility of metagenomic next-generation sequencing for pathogen identification in undiagnosed encephalitis.
Finally, the case provides preliminary evidence supporting combination antiviral therapy in persistent LCMV infection.
The Bottom Line · Clinical Pearl
“Finally, the case provides preliminary evidence supporting combination antiviral therapy in persistent LCMV infection.”
Published in The Lancet Infectious Diseases · Current Stage: Preclinical