Objective: To report a case of Listeria monocytogenes meningitis in a 73-year-old man receiving infliximab for rheumatoid arthritis.
Case Summary: A 73-year-old white man taking infliximab for rheumatoid arthritis developed listeria meningitis following his second dose. He was receiving other immunosuppressants; however, these remained constant immediately prior to the infection. Diagnosis was confirmed with L. monocytogenes isolated in the cerebrospinal fluid. The patient received 21 days of antibiotic therapy and recovered without any complications.
Discussion: L. monocytogenes is a gram-positive, non-spore-forming rod that has been associated with the ingestion of undercooked foods. This organism can cause sepsis or meningitis; however, immunocompromised patients, elderly patients, pregnant women, and neonates appear to be at greater risk for this type of infection. Tumor-necrosis factor-alpha (TNF-alpha) plays an important role in resistance to this type of infection, and listeria infections have been reported in 26 patients receiving TNF-alpha inhibitors. In our patient, the listeria infection occurred following his second course of infliximab, which provides a temporal relationship between the listeria infection and infliximab. However, his underlying rheumatoid arthritis and chronic steroid therapy would also increase his risk for a listeria infection.
Conclusions: The listeria infection in our patient was a possible adverse event of infliximab according to the Naranjo probability scale. Because the majority of listeria infections occur in patients who are immunosuppressed, it would be reasonable to provide education for healthcare professionals on preventing these infections in all patients receiving immunosuppressants, including anti-TNF-alpha therapy. Those at risk due to their underlying health conditions should also be monitored closely.
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http://dx.doi.org/10.1345/aph.1D151 | DOI Listing |
Unlabelled: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. ( ) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during infection and the variation of the response in different macrophage subtypes remain obscure.
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Centro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mexico.
Pathogenic bacteria trigger complex molecular interactions in hosts that are characterized mainly by an increase in reactive oxygen species (ROS) as well as an inflammation-associated response. To counteract oxidative damage, cells respond through protective mechanisms to promote resistance and avoid tissue damage and infection; among these cellular mechanisms the activation or inhibition of the nuclear factor E2-related factor 2 (Nrf2) is frequently observed. The transcription factor Nrf2 is considered the regulator of several hundred cytoprotective and antioxidant genes.
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January 2025
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal.
Wall teichoic acids (WTAs) from the major Gram-positive foodborne pathogen Listeria monocytogenes are peptidoglycan-associated glycopolymers decorated by monosaccharides that, while not essential for bacterial growth, are required for bacterial virulence and resistance to antimicrobials. Here we report the structure and function of a bacterial WTAs rhamnosyltransferase, RmlT, strictly required for L. monocytogenes WTAs rhamnosylation.
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The Affiliated Zhongda Hospital, Clinical Medical College, Southeast University, Nanjing, Jiangsu, China.
Sepsis, a leading cause of mortality in intensive care units worldwide, lacks effective treatments for advanced-stage sepsis. Therefore, understanding the underlying mechanisms of this disease is crucial. This study reveals that invariant natural killer T (iNKT) cells have an opposing role in the progression of sepsis by suppressing regulatory T (Treg) cell differentiation and function.
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December 2024
Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky, USA.
Unlabelled: are facultative intracellular bacterial pathogens that cause foodborne disease in humans. The bacteria can use the surface protein InlA to invade intestinal epithelial cells or transcytose across M cells in the gut, but it is not well understood how the bacteria traffic from the underlying lamina propria to the draining mesenteric lymph nodes (MLN). Previous studies indicated that associated with both monocytes and dendritic cells in the intestinal lamina propria.
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