Prosthetic hip infection due to Campylobacter jejuni.

A woman in her 60s with a left hip prosthesis was presented with left hip pain and fever. She had an elevated white blood cell count and inflammatory markers. Synovial fluid Gram stain demonstrated curved Gram-negative rods identified as Campylobacter jejuni The patient initially refused surgery and after 3 months underwent one-stage exchange after which she was treated with 12 weeks of levofloxacin. Her inflammatory markers normalised and she was clinically doing well at her 6-month follow-up. C. jejuni is a rare cause of prosthetic joint infection and should be included in the differential diagnosis when a patient has risk factors even without significant preceding gastrointestinal symptoms. Per most recent Infectious Diseases Society of America guidelines, treatment after one-stage revision includes 4-6 weeks of intravenous antimicrobials followed by possible oral suppression therapy, while the European guidelines recommend 12 weeks of orally bioavailable antibiotics.

Hemozoin-mediated inflammasome activation limits long-lived anti-malarial immunity.

During acute malaria, most individuals mount robust inflammatory responses that limit parasite burden. However, long-lived sterilizing anti-malarial memory responses are not efficiently induced, even following repeated Plasmodium exposures. Using multiple Plasmodium species, genetically modified parasites, and combinations of host genetic and pharmacologic approaches, we find that the deposition of the malarial pigment hemozoin directly limits the abundance and capacity of conventional type 1 dendritic cells to prime helper T cell responses. Hemozoin-induced dendritic cell dysfunction results in aberrant Plasmodium-specific CD4 T follicular helper cell differentiation, which constrains memory B cell and long-lived plasma cell formation. Mechanistically, we identify that dendritic cell-intrinsic NLRP3 inflammasome activation reduces conventional type 1 dendritic cell abundance, phagocytosis, and T cell priming functions in vivo. These data identify biological consequences of hemozoin deposition during malaria and highlight the capacity of the malarial pigment to program immune evasion during the earliest events following an initial Plasmodium exposure.