Tuberculosis is an ancient disease that humanity struggled with for centuries and continues to struggle with. The bacteria Mycobacterium tuberculosis often infects the lungs through respiratory transmission and manifests itself through various symptoms, including cutaneous infections. Cutaneous tuberculosis (CTB) comprises about 1% to 1.5% of all extrapulmonary manifestations and is often accompanied by polymorphous lesions, including papules, nodules, plaques, ulcers, gummas, and verrucous lesions. CTB is most commonly observed in low-income, HIV, and immunosuppressed populations, similar to intrapulmonary manifestations. The main pathogen for CTB is M. tuberculosis but less commonly with M. bovis and BCG vaccine, and the modes of transmission are largely classified into exogenous and endogenous CTB. Current treatment options for CTB include oral therapy of antibiotic medications such as rifampicin, streptomycin, ethambutol, isoniazid, and pyrazinamide, which is occasionally combined with surgical intervention.

Tuberculosis (TB) caused by Mycobacterium tuberculosis (M.tb) remains a global health crisis, with over 10 million people affected annually. Despite advancements in treatment, M.tb has developed mechanisms to evade host immune responses, complicating efforts to eradicate the disease. Two emerging cell death pathways, ferroptosis and cuproptosis, have been linked to TB pathogenesis. Ferroptosis, an iron-dependent form of cell death, is driven by lipid peroxidation and reactive oxygen species (ROS) accumulation. This process can limit M.tb replication by depleting intracellular iron and inducing macrophage necrosis. However, excessive ferroptosis may lead to tissue damage and aid bacterial dissemination. Cuproptosis, triggered by copper accumulation, disrupts mitochondrial metabolism, leading to protein aggregation and cell death. M.tb exploits both iron and copper metabolism to survive within macrophages, manipulating these processes to resist oxidative stress and immune responses. This review examines the roles of ferroptosis and cuproptosis in TB, discussing how M.tb manipulates these pathways for survival. While therapeutic strategies targeting these processes, such as ferroptosis inducers (Erastin, RSL3) and inhibitors (Ferrostatin-1) and copper ionophores (Disulfiram, Elesclomol) and chelators, show promise, the limited understanding of these pathways and potential off-target effects remains a significant challenge. Further exploration of these pathways may provide insights into the development of targeted therapies aimed at controlling M.tb infection while minimizing host tissue damage. By elucidating the complex interactions between ferroptosis, cuproptosis, and TB, future therapies could better address bacterial resistance and improve clinical outcomes.

As the world continues to suffer from an ever-growing number of confirmed cases of the SARS-CoV-2 novel coronavirus, researchers are at the forefront of developing the best plan to overcome this pandemic through analyzing the pathogenesis, prevention, and treatment options pertaining to the virus. In the midst of a pandemic, the main route for detection of the virus has been conducting antigen tests for rapid results, using qRT-PCR, and conducting more accurate molecular tests, using rRT-PCR, on samples from patients. Most common treatments for those infected with COVID-19 include Remdesivir, an antiviral, dexamethasone, a steroid, and rarely, monoclonal antibody treatments. Although these treatments exist and are used commonly in hospitals all around the globe, clinicians often challenge the efficacy and benefit of these remedies for the patient. Furthermore, targeted therapies largely focus on interfering with or reducing the binding of viral receptors and host cell receptors affected by the SARS-CoV-2 novel coronavirus. In addition to treatment, the most efficacious method of preventing the spread of COVID-19 is the development of multiple vaccines that have been distributed as well as the development of multiple vaccine candidates that are proving hopeful in preventing severe symptoms of the virus. The exaggerated immune response to the virus proves to be a worrying complication due to widespread inflammation and subsequent clinical sequela. The medical and scientific community as a whole will be expected to respond with the latest in technology and research, and further studies into the pathogenesis, clinical implications, identification, diagnosis, and treatment of COVID-19 will push society past this pandemic.