Mouse Anti-Sheep Erythrocyte Hybridoma [TSCD-SG30-2-4]

Infective endocarditis (IE) is a rare cause of multifocal septic arthritis. We report a patient who presented with oligu-articular septic arthritis as a complication of tricuspid valve endocarditis, a rare condition. A 69-year-old female presented to the emergency department with complaints of fever, myalgia, right shoulder, and right knee pain. Initial investigation elaborated on elevated C-reactive protein, erythrocyte sedimentation rate (ESR), and white blood cell. Imaging studies, including X-ray, were unrevealing. Blood cultures came out positive for Methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia. Magnetic resonance imaging (MRI) of the right shoulder and right knee showed joint effusion with soft tissue swelling. Diagnostic arthroscopic washout of right shoulder and right knee showed neutrophilic pleocytosis, and the cultures were positive for MSSA. Despite adequate antibiotic coverage for MSSA bacteremia with ol igoarticular/multifocal septic arthritis, the patient's fever did not resolve. Initial transthoracic echocardiography (TTE) was negative for any vegetation. Transesophageal echocardiography (TEE) showed vegetations on the tricuspid valve with tricuspid regurgitation and was diagnosed with acute bacterial IE. A multi-disciplinary approach was adopted. She underwent tricuspid valve repair with annuloplasty and was treated with nafcillin for six weeks. She successfully recovered from MSSA bacteremia, and follow-up TEE was negative for any vegetations.

It is well established that intracellular pathogens mobilise signalling pathways to manipulate gene expression of their host cell to promote their own survival. Surprisingly, there is evidence that specific host signalling molecules are likewise activated in a-nucleated erythrocytes in response to infection with malaria parasites. In this paper (Adderley et al., Nature Communications 2020), we report the system-wide assessment of host erythrocyte signalling during the course of infection with Plasmodium falciparum. This was achieved through the use of antibody microarrays containing >800 antibodies directed against human signalling proteins, which enabled us to interrogate the status of host erythrocyte signalling pathways at the ring, trophozoite and schizont stages of parasite development. This not only confirmed the pre-existing fragmentary data on the activation of a host erythrocyte PAK-MEK pathway, but also identified dynamic changes to many additional signalling elements, with trophozoite-infected erythrocytes displaying the largest mobilisation of host cell signalling. This study generated a comprehensive dataset on the modulation of host erythrocyte signalling during infection with P. falciparum, and provides the proof of principle that human protein kinases activated by Plasmodium infection represent attractive targets for antimalarial intervention.