Systemic lupus erythematosus (SLE) is a systemic autoimmune condition with many clinical presentations. It is classically seen in young to middle-aged females and can present with cutaneous, renal, serosal, hematological, joint, and/or neurological manifestations at the time of diagnosis or may develop over the course of the disease. Late-onset SLE or SLE in the elderly is a subtype that differs from the classic SLE in age group, clinical presentation, involvement of organs, and severity. Here, we present the case of a geriatric Hispanic male noted to have worsening renal function. The patient was diagnosed with lupus nephritis (LN) upon obtaining serological markers and renal biopsy. LN, a renal sequela of SLE, presents with a full-house immunofluorescence pattern. LN, along with high titers of the antinuclear antibody (ANA) and/or anti-double-stranded DNA (anti-dsDNA) antibody, is an effective tool to diagnose SLE in patients without extrarenal manifestations of the disease. The patient was managed with glucocorticoids and mycophenolate mofetil therapy, which led to a rapid downtrend of creatinine, resulting in stabilization of renal function and deferring the need for a hemodialysis. This case highlights the topic of late-onset SLE presenting with LN in geriatric patients.

Neurotropic viruses are a threat to human populations due to ongoing zoonosis. A wide array of neurological manifestations can occur most often including parkinsonism, encephalitis/encephalopathy, flaccid myelitis, and Guillain-Barré syndrome. Neuroinvasion occurs through: transneural transmission, blood brain barrier (BBB) dysfunction, and ‘trojan horse’ mechanism or infected immune cell trafficking into the central nervous system (CNS). Transneural transmission occurs through virus mediated hijacking of intracellular transport proteins allowing retrograde viral transport. BBB dysfunction occurs through cytokine storm increasing membrane permissibility. Increased chemokine expression allows leukocyte trafficking to the BBB. Virally infected leukocytes may successfully pass through the BBB allowing the pathogen to infect microglia and other CNS cell types. We define cerebrospinal fluid (CSF) nondetection as a virus’ ability to evade direct CSF detection but still causing significant neurological symptoms and disease. Mechanisms of CSF nondetection include: transneuronal propagation through trans-synaptic transmission, and synaptic microfusion, as well as intrathecal antibody synthesis and virus neutralization. Direct virus detection in CSF is associated with an increased neurological disease burden. However, the lack of CSF detection does not exclude CNS involvement due to possible neuroevasive mechanisms.