Glaucoma causes irreversible vision loss, with elevated intraocular pressure (IOP) being the only known modifiable risk factor. There are a variety of medical and interventional options for lowering IOP; however, despite these treatments, glaucoma continues to be a leading cause of visual impairment. Further research continues to strive for treatment options with improved side effect profiles, additional IOP-lowering effects, and ease of use. This review provides a brief summary of current IOP-lowering therapies and then outlines pipeline ocular hypotensive agents, their mechanisms of action, benefits, and side effect profiles. Advancements are seen within currently used eye drop classes such as prostaglandin analogues, Rho kinase inhibitors and nitric oxide donors, whilst there are also new drug classes, such as tyrosine protein kinase activators. Most developing drugs are topical drop formulations, with a number already having entered Phase III trials. Alternative drug delivery methods are also in development and will be briefly discussed. Pharmacological and drug delivery developments continue to provide glaucoma patients and clinicians with new options and the promise of better outcomes, particularly in terms of improved tolerance and reduced frequency of dosing.

Systemic dissemination and peri-prosthetic infection of Mycobacterium bovis (M. bovis) following intravesical Bacillus Calmette-Guerin (BCG) therapy presents a rare but significant complication of treatment for non-muscle invasive bladder carcinoma. We present a patient with Mycobacterium bovis infection of a prosthetic hip nine months following BCG therapy for bladder cancer. The debridement and (implant) prosthesis retention approach in conjunction with anti-tuberculous medication (DAIR) employed in this case, allowed the same prosthesis to be retained. This case report highlights the importance of physician awareness of the possibility BCG peri-prosthetic infections.

Ethambutol is utilised in the treatment of and infection. The authors report two siblings who developed the adverse effect of ethambutol-induced optic chiasmopathy, with recovery following cessation of ethambutol. Discussion explores potential genetic predisposition to development of this condition and its resolution. Ethambutol optic neuropathy (EON), Leber's hereditary optic neuropathy (LHON), and other optic neuropathies of mitochondrial origin share a common pathophysiology. Consequently, the authors postulate treatments utilised in LHON, including vitamin B supplementation and idebenone, may have benefit in EON. This article presents concepts for further research, suggesting a potential genetic susceptibility to EON and its treatment.