A Rare Case of Prosthetic Joint Infection with Streptococcus gordonii.

BACKGROUND Chronic prosthetic joint infection (PJI) is a devastating complication following total joint arthroplasty, resulting in significant morbidity and mortality. The criterion standard of treatment for chronic PJI is two-stage revision arthroplasty consisting of complete hardware removal, thorough irrigation and debridement, placement of an antibiotic spacer, prolonged intravenous antibiotics based on culture sensitivities, and revision total knee arthroplasty once the infection resolves. The most common organism implicated in chronic PJI is Staphylococcus aureus. CASE REPORT In this report, we have summarized the case of a 75-year-old woman who developed chronic PJI caused by an unusual organism, Streptococcus gordonii, 1 year after a right total knee arthroplasty. S. gordonii is a gram-positive organism that is an oral flora and a colonizer of human teeth. This organism is known to create biofilm on the human teeth, more commonly known as dental plaque. S. gordonii has the ability to travel to extraoral sites and cause infection. It has been found to be a cause of subacute bacterial endocarditis, but it has been rarely described in the literature as a cause of prosthetic joint infection. Treatment of S. gordonii requires a tailored approach. CONCLUSIONS This case report highlights the clinical presentation, diagnosis, and treatment of chronic prosthetic joint infection caused by S. gordonii and identifies a rare cause of PJI that is not well documented in the literature. Streptococcal PJI portends a poorer prognosis, and identification of this organism is crucial for prompt treatment and improved outcomes for PJI.

A Rare Case of Raoultella planticola and Enterococcus casseliflavus Coinfection.

Raoultella planticola, a Gram-negative bacterium, is a nonmotile rod usually found in soil and aquatic environments. It can be found in association with gastrointestinal malignancy. Enterococcus casseliflavus is a rare vancomycin-resistant Enterococcus that is responsible for some bacteremia. Our case describes a unique presentation of colonization with both R. planticola and E. casseliflavus isolated from the biliary stent isolates of a patient with known pancreatic malignancy and concomitant E. casseliflavus bacteremia. This is the first case ever reported of infection with both species.

Actin polymerization controls cilia-mediated signaling.

Primary cilia are polarized organelles that allow detection of extracellular signals such as Hedgehog (Hh). How the cytoskeleton supporting the cilium generates and maintains a structure that finely tunes cellular response remains unclear. Here, we find that regulation of actin polymerization controls primary cilia and Hh signaling. Disrupting actin polymerization, or knockdown of N-WASp/Arp3, increases ciliation frequency, axoneme length, and Hh signaling. Cdc42, a potent actin regulator, recruits both atypical protein pinase C iota/lambda (aPKC) and Missing-in-Metastasis (MIM) to the basal body to maintain actin polymerization and restrict axoneme length. Transcriptome analysis implicates the Src pathway as a major aPKC effector. aPKC promotes whereas MIM antagonizes Src activity to maintain proper levels of primary cilia, actin polymerization, and Hh signaling. Hh pathway activation requires Smoothened-, Gli-, and Gli1-specific activation by aPKC. Surprisingly, longer axonemes can amplify Hh signaling, except when aPKC is disrupted, reinforcing the importance of the Cdc42-aPKC-Gli axis in actin-dependent regulation of primary cilia signaling.