ABSTRACT
Rabies, a millennia-old viral infection transmitted through animal bites, poses a lethal threat to humans, with a historic fatality rate of 100% if left untreated. Louis Pasteur's introduction of the rabies vaccine in 1885 marked a turning point in the battle against rabies, preventing numerous cases. The purpose of this paper is to review the historical development, current challenges, and future prospects of rabies vaccination and treatment, with emphasis on the importance of continued research and collaborative efforts in the quest to eradicate this deadly infection. Historical vaccine development progressed from inactivated to live-attenuated forms, with modern recombinant techniques showing promise. The preventive measures at present primarily involve vaccination, but challenges persist, such as differing safety profiles and immunogenicity among vaccine types. Pre-exposure prophylaxis with a three-dose vaccine series is crucial, especially in high-risk scenarios. Post-exposure prophylaxis combines human rabies immunoglobulin and inactivated rabies virus vaccine. The quest for the next generation of vaccines explores genetically modified and viral vector-based approaches; emerging treatments include gene therapy, virus-like particles, and monoclonal antibodies, offering hope for improved outcomes. Economic barriers to post-exposure prophylaxis, limited education, and awareness challenge rabies control. Cost-effective solutions and comprehensive awareness campaigns are vital for the successful eradication of rabies. More research and collaborative endeavors remain pivotal in the ongoing journey to eradicate rabies, one of the deadliest infectious diseases known to humans, if not met with prophylactic measures.
ABSTRACT
Coccidioidomycosis, also termed Valley fever, is a fungal infection caused by the inhalation of Coccidioides endospores. Once inhaled by a human host, the arthroconidia endospores travel to the lungs' alveoli to transform into spherules that grow and rupture to release more endospores. In the host immune response, macrophages, neutrophils, and dendritic cells will recognize the fungal antigen, producing pro-inflammatory cytokine. Th2 lymphocytes (type 2 helper T cells) are theorized to be the main human defense against Coccidioides given that Th2 deficiency is seen in patients with disseminated forms of the disease. A common triad of symptoms of coccidioidomycosis, also called "desert rheumatism," include fever, erythema nodosum, and arthralgia, often accompanied by a respiratory problem. In a clinical setting, along with the evaluation of symptoms, a medical provider may also test the patient's blood using antibody tests or perform microscopy to directly detect the presence of Coccidioides in a patient tissue sample for confirmation of a diagnosis. Imaging modalities may also be used to determine lung involvement and assess disease progression. A majority of coccidioidomycosis cases do not require specific treatment and will resolve on their own, so an approach with symptomatic treatment in mind is appropriate. If symptoms do not resolve, azoles or amphotericin B may be used, with the standard drug of choice being fluconazole (Diflucan, Pfizer, New York, New York, United States). Treatment varies depending on the immunocompetency of the patient. To name a few, pregnant patients and those with history of human immunodeficiency virus (HIV) or transplantation require special considerations.
