臨床感染症: オープンアクセス

Tuberculosis (TB) remains a significant global health challenge, particularly in high-burden regions. The emergence of Multi-Drug Resistant Tuberculosis (MDR-TB) complicates treatment strategies and exacerbates public health concerns. Molecular epidemiology provides critical insights into the transmission dynamics, genetic diversity and resistance mechanisms of MDR-TB, enabling more targeted and effective interventions. Tuberculosis is an infectious disease caused by the bacterium Mycobacterium tuberculosis. Despite significant advances in medicine and public health, TB remains a major global health concern, particularly in low- and middle-income countries. Understanding the epidemiology, diagnosis, treatment and prevention of TB is crucial for effective control and eventual eradication of this disease. TB is one of the top 10 causes of death worldwide and the leading cause of death from a single infectious agent, ranking above HIV/AIDS.

While the acute phase of Zika infection often presents with mild symptoms or none at all in adults, its long-term effects, especially on neurological and developmental outcomes, have raised significant concerns. Zika virus, primarily transmitted through the bite of infected Aedes mosquitoes, gained prominence during the 2015-2016 outbreak in the Americas. Since its emergence as a global health concern, the Zika virus has captured international attention due to its association with devastating neurological complications, particularly in infants born to infected mothers. What made Zika particularly alarming was its link to Congenital Zika Syndrome (CZS), characterized by microcephaly, brain calcifications and other neurological abnormalities in newborns. Additionally, Zika has been associated with Guillain-Barre Syndrome (GBS) in adults, an autoimmune disorder affecting the peripheral nervous system.

Over the past few decades, significant strides have been made in understanding how host genetics influence vulnerability to infectious diseases, shedding light on both individual and population-level susceptibilities. This exploration has not only deepened our understanding of disease mechanisms but also paved the way for personalized approaches to treatment and prevention. Human susceptibility to infectious diseases is not solely determined by one gene but is rather a complex interplay of multiple genetic factors. Variations in genes encoding various components of the immune system, such as receptors, cytokines and other immune response mediators, can significantly impact an individual's ability to fend off pathogens. In the intricate dance between pathogens and humans, susceptibility to infectious diseases often seems unpredictable. While environmental factors play a significant role, the genetic makeup of the host also plays a crucial part in determining susceptibility.

Clostridioides difficile stands out as a formidable pathogen, notorious for causing debilitating infections. Understanding the dynamic interplay between gut microbiota and C. difficile is pivotal in elucidating the pathogenesis and devising effective management strategies for this challenging infection. Clostridioides difficile Infection (CDI) typically arises following disruption of the gut microbiota, often due to antibiotic therapy. Antibiotics disturb the delicate balance of microbial communities in the gut, providing an opportunity for C. difficile to proliferate and produce toxins, namely, toxin A and toxin B, which are primary virulence factors responsible for the clinical manifestations of CDI. In the intricate landscape of the human body, trillions of microbes coexist, with the gut microbiota being a crucial player in maintaining health and homeostasis. Among the myriad of microorganisms residing in the gut, These toxins lead to inflammation and damage to the intestinal epithelium, resulting in symptoms ranging from mild diarrhea to severe colitis and potentially life-threatening complications such as toxic megacolon.