Background Pleurostomophora richardsiae (formerly Phialophora richardsiae) is a dematiaceous fungus that is an uncommon cause of ocular infection. Herein, we present a case of endogenous endophthalmitis associated with disseminated P. richardsiae infection.FindingsThis is a descriptive case report with a brief review of literature. A 43-year-old male admitted to the hospital following an acute cerebellar hemorrhage was found to have a swollen and tender wrist. The patient was afebrile with leukocytosis. Visual acuity was hand motion in the right eye and 20/20 in the left. Right eye examination noted anterior chamber cells and flare, vitreous haze and multiple large, and fluffy retinal infiltrates. Diagnostic vitrectomy revealed a mixed inflammatory cell infiltrate with numerous fungal elements. Blood cultures were negative, multiple transesophageal echocardiography studies revealed no vegetations, and synovial fluid aspiration of the wrist and biopsy of the radius were unremarkable. The patient was treated with intravitreal cefazolin, vancomycin, and amphotericin B, topical ciprofloxacin and natamycin, and intravenous amphotericin B and voriconazole. Visual acuity in the right eye declined to light perception, and examination revealed increasing anterior and posterior chamber inflammation. The patient died several weeks after presentation due to a massive intracranial hemorrhage. Fungal culture results from the vitrectomy were received post mortem and were positive for P. richardsiae.Conclusions P. richardsiae endophthalmitis is rare, and outcomes are typically poor. Infections typically occur following traumatic skin inoculation; however, a long refractory period may occur before symptoms develop. Early diagnosis and combination antimicrobial therapy are essential to optimize visual outcomes.

P2Y(12) receptor antagonism inhibits platelet aggregation by preventing adenosine diphosphate (ADP)-mediated amplification of activation pathways downstream of primary agonists, such as thrombin and collagen. However, the role of ADP signaling in maintaining aggregate stability and the effects of P2Y(12) antagonists on preestablished aggregates in vitro and arterial thrombus in vivo are not well understood. This study evaluated the impact of P2Y(12) signaling on platelet aggregate stability and early thrombotic occlusion using a reversible P2Y(12) antagonist, ticagrelor. There were 2 study objectives: (1) to determine if there was a time-dependent factor on the capacity of a P2Y(12) antagonist to affect human platelet aggregate stability in vitro using light transmission aggregometry and (2) to evaluate the extent of arterial thrombus reversal in a preclinical model upon administration of ticagrelor in vivo. Platelet aggregates were exposed to ticagrelor after ADP or collagen activation, monitored for stability by aggregometry, and visualized by microscopy. Freshly formed ADP- and collagen-induced platelet aggregates were more rapidly dispersed by a P2Y(12) antagonist than drug carrier control at clinically relevant concentrations (P < 0.05). However, stable aggregates were not noticeably affected. A murine arterial thrombosis model was used to evaluate thrombus stability in an in vivo mouse model. Thrombotic occlusion was induced by FeCl(3), followed by a bolus intravenous administration of ticagrelor or vehicle control. Doppler blood flow was monitored before injury and 30 minutes after bolus administration. Arteries were retrieved for inspection for residual thrombus. Early arterial thrombotic occlusion in vivo was partially reversed by ticagrelor administration. Blood flow through the injured artery increased, and thrombus size within the artery decreased (P < 0.05, n = 3). In conclusion, P2Y(12) antagonism disrupts the stability of newly formed platelet aggregates, promoting disaggregation, and reverses thrombotic vascular occlusion. Thus, in addition to activating platelets, signaling via P2Y(12) seems to be required for stabilizing platelet thrombi.

Impairment in trigeminal nerve function causes a loss of corneal sensation and can lead to neurotrophic keratitis (NK). This gradual deterioration in the surface integrity of the cornea predisposes to the development of ulcers and may even progress to perforation, posing a risk for profound vision loss. Many common ophthalmic and systemic conditions, such as herpetic infections, ocular surgeries, neurosurgical procedures, multiple sclerosis and diabetes, can elicit NK by injuring the trigeminal nerve. Disease progression can occur rapidly and without symptoms, therefore, detecting NK early is critical. Management aims to halt continuing corneal damage and promote epithelial cell healing and nerve fibre regeneration. Novel treatment options show promise in restoring corneal sensitivity by re-establishing innervation, targeting the fundamental source of NK.

The frontalis suspension procedure is a common surgical method for patients with severe blepharoptosis. While frontalis

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